👤 Shurong Yang

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Also published as: A Yang, A-Li Yang, Acong Yang, Ai-Lun Yang, Aige Yang, Airong Yang, Aiting Yang, Aizhen Yang, Albert C Yang, Alex J T Yang, An-Qi Yang, Andrew Yang, Angang Yang, Angela Wei Hong Yang, Anni Yang, Aram Yang, B Yang, Baigao Yang, Baixia Yang, Bangjia Yang, Bao Yang, Baofeng Yang, Baoli Yang, Baoxin Yang, Baoxue Yang, Bei Yang, Beibei Yang, Biao Yang, Bin Q Yang, Bin Yang, Bing Xiang Yang, Bing Yang, Bingyu Yang, Bo Yang, Bohui Yang, Boo-Keun Yang, Bowen Yang, Boya Yang, Burton B Yang, Byoung Chul Yang, Caimei Yang, Caixia Yang, Caixian Yang, Caixin Yang, Can Yang, Canchai Yang, Ce Yang, Celi Yang, Chan Mo Yang, Chan-Mo Yang, Chang Yang, Chang-Hao Yang, Changheng Yang, Changqing Yang, Changsheng Yang, Changwei Yang, Changyun Yang, Chanjuan Yang, Chao Yang, Chao-Yuh Yang, Chaobo Yang, Chaofei Yang, Chaogang Yang, Chaojie Yang, Chaolong Yang, Chaoping Yang, Chaoqin Yang, Chaoqun Yang, Chaowu Yang, Chaoyun Yang, Chaozhe Yang, Chen Die Yang, Chen Yang, Cheng Yang, Cheng-Gang Yang, Chengfang Yang, Chenghao Yang, Chengkai Yang, Chengkun Yang, Chengran Yang, Chenguang Yang, Chengyingjie Yang, Chengzhang Yang, Chensi Yang, Chensu Yang, Chenxi Yang, Chenyu Yang, Chenzi Yang, Chi Yang, Chia-Wei Yang, Chieh-Hsin Yang, Chien-Wen Yang, Chih-Hao Yang, Chih-Min Yang, Chih-Yu Yang, Chihyu Yang, Ching-Fen Yang, Ching-Wen Yang, Chongmeng Yang, Chuan He Yang, Chuan Yang, Chuanbin Yang, Chuang Yang, Chuanli Yang, Chuhu Yang, Chun Yang, Chun-Chun Yang, Chun-Mao Yang, Chun-Seok Yang, Chunbaixue Yang, Chung-Hsiang Yang, Chung-Shi Yang, Chung-Yi Yang, Chunhua Yang, Chunhui Yang, Chunjie Yang, Chunjun Yang, Chunlei Yang, Chunli Yang, Chunmao Yang, Chunping Yang, Chunqing Yang, Chunru Yang, Chunxiao Yang, Chunyan Yang, Chunyu Yang, Congyi Yang, Cui Yang, Cuiwei Yang, Cunming Yang, Dai-Qin Yang, Dan Yang, Dan-Dan Yang, Dan-Hui Yang, Dandan Yang, Danlu Yang, Danrong Yang, Danzhou Yang, Dapeng Yang, De-Hua Yang, De-Zhai Yang, Decao Yang, Defu Yang, Deguang Yang, Dehao Yang, Dehua Yang, Dejun Yang, Deli Yang, Dengfa Yang, Deok Chun Yang, Deshuang Yang, Di Yang, Dianqiang Yang, Ding Yang, Ding-I Yang, Diya Yang, Diyuan Yang, Dong Yang, Dong-Hua Yang, Dongfeng Yang, Dongjie Yang, Dongliang Yang, Dongmei Yang, Dongren Yang, Dongshan Yang, Dongwei Yang, Dongwen Yang, DuJiang Yang, Eddy S Yang, Edwin Yang, Ei-Wen Yang, Emily Yang, Enlu Yang, Enzhi Yang, Eric Yang, Eryan Yang, Ethan Yang, Eunho Yang, Fajun Yang, Fan Yang, Fang Yang, Fang-Ji Yang, Fang-Kun Yang, Fei Yang, Feilong Yang, Feiran Yang, Feixiang Yang, Fen Yang, Feng Yang, Feng-Ming Yang, Feng-Yun Yang, Fengjie Yang, Fengjiu Yang, Fengjuan Yang, Fenglian Yang, Fengling Yang, Fengping Yang, Fengying Yang, Fengyong Yang, Fu Yang, Fude Yang, Fuhe Yang, Fuhuang Yang, Fumin Yang, Fuquan Yang, Furong Yang, Fuxia Yang, Fuyao Yang, G Y Yang, G Yang, Gan Yang, Gang Yang, Gangyi Yang, Gao Yang, Gaohong Yang, Gaoxiang Yang, Ge Yang, Gong Yang, Gong-Li Yang, Grace H Y Yang, Guan Yang, Guang Yang, Guangdong Yang, Guangli 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Hongyan Yang, Hongyu Yang, Hongyuan Yang, Hongyue Yang, Howard H Yang, Howard Yang, Hsin-Chou Yang, Hsin-Jung Yang, Hsin-Sheng Yang, Hua Yang, Hua-Yuan Yang, Huabing Yang, Huafang Yang, Huaijie Yang, Huan Yang, Huanhuan Yang, Huanjie Yang, Huanming Yang, Huansheng Yang, Huanyi Yang, Huarong Yang, Huaxiao Yang, Huazhao Yang, Hui Yang, Hui-Ju Yang, Hui-Li Yang, Hui-Ting Yang, Hui-Yu Yang, Hui-Yun Yang, Huifang Yang, Huihui Yang, Huijia Yang, Huijie Yang, Huiping Yang, Huiran Yang, Huixia Yang, Huiyu Yang, Hung-Chih Yang, Hwai-I Yang, Hye Jeong Yang, Hyerim Yang, Hyun Suk Yang, Hyun-Sik Yang, Ill Yang, Ivana V Yang, J S Yang, J Yang, James Y Yang, Jaw-Ji Yang, Jee Sun Yang, Jenny J Yang, Jerry Yang, Ji Hye Yang, Ji Yang, Ji Yeong Yang, Ji-chun Yang, Jia Yang, Jia-Ling Yang, Jia-Ying Yang, Jiahong Yang, Jiahui Yang, Jiajia Yang, Jiakai Yang, Jiali Yang, Jialiang Yang, Jian Yang, Jian-Bo Yang, Jian-Jun Yang, Jian-Ming Yang, Jian-Ye Yang, JianHua Yang, JianJun Yang, Jianbo Yang, Jiang-Min Yang, Jiang-Yan Yang, Jianing Yang, Jianke Yang, Jianli Yang, Jianlou Yang, Jianmin Yang, Jianming Yang, Jianqi Yang, Jianwei Yang, Jianyu Yang, Jiao Yang, Jiarui Yang, Jiawei Yang, Jiaxin Yang, Jiayan Yang, Jiayi Yang, Jiaying Yang, Jiayue Yang, Jichun Yang, Jie Yang, Jie-Cheng Yang, Jie-Hong Yang, Jie-Kai Yang, Jiefeng Yang, Jiehong Yang, Jieping Yang, Jiexiang Yang, Jihong Yang, Jimin Yang, Jin Yang, Jin-Jian Yang, Jin-Kui Yang, Jin-gang Yang, Jin-ju Yang, Jinan Yang, Jinfeng Yang, Jing Yang, Jing-Quan Yang, Jing-Yu Yang, Jingang Yang, Jingfeng Yang, Jinggang Yang, Jinghua Yang, Jinghui Yang, Jingjing Yang, Jingmin Yang, Jingping Yang, Jingran Yang, Jingshi Yang, Jingwen Yang, Jingya Yang, Jingyan Yang, Jingyao Yang, Jingye Yang, Jingyu Yang, Jingyun Yang, Jingze Yang, Jinhua Yang, Jinhui Yang, Jinjian Yang, Jinpeng Yang, Jinru Yang, Jinshan Yang, Jinsong Yang, Jinsung Yang, Jinwen Yang, Jinzhao Yang, Jiong Yang, Ju Dong Yang, Ju Young Yang, Juan Yang, Juesheng Yang, Jumei Yang, Jun J Yang, Jun Yang, Jun-Hua Yang, Jun-Xia Yang, Jun-Xing Yang, Junbo Yang, Jung Dug Yang, Jung Wook Yang, Jung-Ho Yang, Junhan Yang, Junjie Yang, Junlin Yang, Junlu Yang, Junping Yang, Juntao Yang, Junyao Yang, Junyi Yang, Kai Yang, Kai-Chien Yang, Kai-Chun Yang, Kaidi Yang, Kaifeng Yang, Kaijie Yang, Kaili Yang, Kailin Yang, Kaiwen Yang, Kang Yang, Kang Yi Yang, Kangning Yang, Karen Yang, Ke Yang, Keming Yang, Keping Yang, Kexin Yang, Kuang-Yao Yang, Kui Yang, Kun Yang, Kunao Yang, Kunqi Yang, Kunyu Yang, Kuo Tai Yang, L Yang, Lamei Yang, Lan Yang, Le Yang, Lei Yang, Lexin Yang, Leyi Yang, Li Chun Yang, Li Yang, Li-Kun Yang, Li-Qin Yang, Li-li Yang, LiMan Yang, Lian-he Yang, Liang Yang, Liang-Yo Yang, Liangbin Yang, Liangle Yang, Liangliang Yang, Lichao Yang, Lichuan Yang, Licong Yang, Liehao Yang, Lihong Yang, Lihua Yang, Lihuizi Yang, Lijia Yang, Lijie Yang, Lijuan Yang, Lijun Yang, Lili Yang, Lin Sheng Yang, Lin Yang, Lina Yang, Ling Ling Yang, Ling Yang, Lingfeng Yang, Lingling Yang, Lingzhi Yang, Linlin Yang, Linnan Yang, Linqing Yang, Linquan Yang, Lipeng Yang, Liping Yang, Liting Yang, Liu Yang, Liu-Kun Yang, LiuMing Yang, Liuliu Yang, Liwei Yang, Lixian Yang, Lixue Yang, Long In Yang, Long Yang, Long-Yan Yang, Longbao Yang, Longjun Yang, Longyan Yang, Lu M Yang, Lu Yang, Lu-Hui Yang, Lu-Kun Yang, Lu-Qin Yang, Luda Yang, Man Yang, Manqing Yang, Maojie Yang, Maoquan Yang, Mei Yang, Meichan Yang, Meihua Yang, Meili Yang, Meiting Yang, Meixiang Yang, Meiying Yang, Meng Yang, Menghan Yang, Menghua Yang, Mengjie Yang, Mengli Yang, Mengliu Yang, Mengmeng Yang, Mengsu Yang, Mengwei Yang, Mengying Yang, Miaomiao Yang, Mickey Yang, Min Hee Yang, Min Yang, Mina Yang, Ming Yang, Ming-Hui Yang, Ming-Yan Yang, Minghui Yang, Mingjia Yang, Mingjie Yang, Mingjun Yang, Mingli Yang, Mingqian Yang, Mingshi Yang, Mingyan Yang, Mingyu Yang, Minyi Yang, Misun Yang, Mu Yang, Muh-Hwa Yang, Na Yang, Nan Yang, Nana Yang, Nanfei Yang, Neil V Yang, Ni Yang, Ning Yang, Ningjie Yang, Ningli Yang, Pan Yang, Pan-Chyr Yang, Paul Yang, Peichang Yang, Peiran Yang, Peiyan Yang, Peiying Yang, Peiyuan Yang, Peizeng Yang, Peng Yang, Peng-Fei Yang, PengXiang Yang, Pengfei Yang, Penghui Yang, Pengwei Yang, Pengyu Yang, Phillip C Yang, Pin Yang, Ping Yang, Ping-Fen Yang, Pinghong Yang, Pu Yang, Q H Yang, Q Yang, Qi Yang, Qi-En Yang, Qian Yang, Qian-Jiao Yang, Qian-Li Yang, QianKun Yang, Qiang Yang, Qianhong Yang, Qianqian Yang, Qianru Yang, Qiaoli Yang, Qiaorong Yang, Qiaoyuan Yang, Qifan Yang, Qifeng Yang, Qiman Yang, Qimeng Yang, Qiming Yang, Qin Yang, Qinbo Yang, Qing Yang, Qing-Cheng Yang, Qingcheng Yang, Qinghu Yang, Qingkai Yang, Qinglin Yang, Qingling Yang, Qingmo Yang, Qingqing Yang, Qingtao Yang, Qingwu Yang, Qingya Yang, Qingyan Yang, Qingyi Yang, Qingyu Yang, Qingyuan Yang, Qiong Yang, Qiu Yang, Qiu-Yan Yang, Qiuhua Yang, Qiuhui Yang, Qiulan Yang, Qiuli Yang, Qiuxia Yang, Qiwei Yang, Qiwen Yang, Quan Yang, Quanjun Yang, Quanli Yang, Qun-Fang Yang, R Yang, Ran Yang, Ren-Zhi Yang, Renchi Yang, Renhua Yang, Renjun Yang, Renqiang Yang, Renzhi Yang, Ri-Yao Yang, Richard K Yang, Robert Yang, Rong Yang, Rongrong Yang, Rongxi Yang, Rongyuan Yang, Rongze Yang, Rui Xu Yang, Rui Yang, Rui-Xu Yang, Rui-Yi Yang, Ruicheng Yang, Ruifang Yang, Ruihua Yang, Ruilan Yang, Ruili Yang, Ruiqin Yang, Ruirui Yang, Ruiwei Yang, Rulai Yang, Ruming Yang, Run Yang, Runjun Yang, Runxu Yang, Runyu Yang, Runzhou Yang, Ruocong Yang, Ruoyun Yang, Ruyu Yang, S J Yang, Se-Ran Yang, Sen Yang, Senwen Yang, Seung Yun Yang, Seung-Jo Yang, Seung-Ok Yang, Shan Yang, Shangchen Yang, Shanghua Yang, Shangwen Yang, Shanzheng Yang, Shao-Hua Yang, Shaobin Yang, Shaohua Yang, Shaoling Yang, Shaoqi Yang, Shaoqing Yang, Sheng Sheng Yang, Sheng Yang, Sheng-Huei Yang, Sheng-Qian Yang, Sheng-Wu Yang, ShengHui Yang, Shenglin Yang, Shengnan Yang, Shengqian Yang, Shengyong Yang, Shengzhuang Yang, Shenhui Yang, Shi-Ming Yang, Shiaw-Der Yang, Shifeng Yang, Shigao Yang, Shijie Yang, Shiming Yang, Shipeng Yang, Shiping Yang, Shiu-Ju Yang, Shiyi Yang, Shizhong Yang, Shizhuo Yang, Shu Yang, ShuSheng Yang, Shuai Yang, Shuaibing Yang, Shuaini Yang, Shuang Yang, Shuangshuang Yang, Shucai Yang, Shufang Yang, Shuhua Yang, Shujuan Yang, Shujun Yang, Shulan Yang, Shulin Yang, Shuming Yang, Shun-Fa Yang, Shuo Yang, Shuofei Yang, Shuping Yang, Shuqi Yang, Shuquan Yang, Shushen Yang, Shuye Yang, Shuyu Yang, Si Yang, Si-Fu Yang, Sibao Yang, Sibo Yang, Sichong Yang, Sihui Yang, Sijia Yang, Siqi Yang, Sirui Yang, Sisi Yang, Sitao Yang, Siwen Yang, Siyi Yang, Siyu Yang, Sizhen Yang, Sizhu Yang, Song Yang, Song-na Yang, Songpeng Yang, Songye Yang, Soo Hyun Yang, Su Yang, Su-Geun Yang, Suhong Yang, Sujae Yang, Sujuan Yang, Suk-Kyun Yang, Sun Kyung Yang, Suwol Yang, Suxia Yang, Suyi Yang, Suyu Yang, Tai-Hui Yang, Tailai Yang, Tao Yang, Tengyun Yang, Thomas P Yang, Ti Yang, Tian Yang, Tianbao Yang, Tianfeng Yang, Tianjie Yang, Tianmin Yang, Tianpeng Yang, Tianqiong Yang, Tiantian Yang, Tianxin Yang, Tianyou Yang, Tianyu Yang, Tianze Yang, Tianzhong Yang, Ting Yang, Ting-Xian Yang, Tingting Yang, Tingyu Yang, Tong Yang, Tong Yi Yang, Tong-Xin Yang, Tonglin Yang, Tongren Yang, Tuanmin Yang, Ueng-Cheng Yang, W Yang, Wan-Chen Yang, Wan-Jung Yang, Wang Yang, Wannian Yang, Wei Qiang Yang, Wei Yang, Wei-Fa Yang, Wei-Xin Yang, Weidong Yang, Weiguang Yang, Weihan Yang, Weijian Yang, Weili Yang, Weimin Yang, Weiran Yang, Weiwei Yang, Weixian Yang, Weizhong Yang, Wen Yang, Wen Z Yang, Wen-Bin Yang, Wen-Chin Yang, Wen-He Yang, Wen-Hsuan Yang, Wen-Ming Yang, Wen-Wen Yang, Wen-Xiao Yang, WenKai Yang, Wenbo Yang, Wenchao Yang, Wending Yang, Wenfei Yang, Wenhong Yang, Wenhua Yang, Wenhui Yang, Wenjian Yang, Wenjie Yang, Wenjing Yang, Wenjuan Yang, Wenjun Yang, Wenli Yang, Wenlin Yang, Wenming Yang, Wenqin Yang, Wenshan Yang, Wentao Yang, Wenwen Yang, Wenwu Yang, Wenxin Yang, Wenxing Yang, Wenying Yang, Wenzhi Yang, Wenzhu Yang, William Yang, Woong-Suk Yang, Wu Yang, Wu-de Yang, X Yang, X-J Yang, Xi Yang, Xi-You Yang, Xia Yang, Xian Yang, Xiang Yang, Xiang-Hong Yang, Xiang-Jun Yang, Xianggui Yang, Xianghong Yang, Xiangliang Yang, Xiangling Yang, Xiangqiong Yang, Xiangxiang Yang, Xiangyu Yang, Xiao Yang, Xiao-Dong Yang, Xiao-Fang Yang, Xiao-Hong Yang, Xiao-Jie Yang, Xiao-Juan Yang, Xiao-Meng Yang, Xiao-Ming Yang, Xiao-Qian Yang, Xiao-Yan Yang, Xiao-Ying Yang, Xiao-Yu Yang, Xiao-guang Yang, XiaoYan Yang, Xiaoao Yang, Xiaobin Yang, Xiaobo Yang, Xiaochen Yang, Xiaodan Yang, Xiaodi Yang, Xiaodong Yang, Xiaofei Yang, Xiaofeng Yang, Xiaohao Yang, Xiaohe Yang, Xiaohong R Yang, Xiaohong Yang, Xiaohuang Yang, Xiaohui Yang, Xiaojian Yang, Xiaojie Yang, Xiaojing Yang, Xiaojuan Yang, Xiaojun Yang, Xiaoli Yang, Xiaolu Yang, Xiaomeng Yang, Xiaoming Yang, Xiaonan Yang, Xiaoping Yang, Xiaoqian Yang, Xiaoqin Yang, Xiaoqun Yang, Xiaorong Yang, Xiaoshan Yang, Xiaoshi Yang, Xiaosong Yang, Xiaotian Yang, Xiaotong Yang, Xiaowei Yang, Xiaowen Yang, Xiaoxiao Yang, Xiaoxin Yang, Xiaoxu Yang, Xiaoyao Yang, Xiaoyi Yang, Xiaoyong Yang, Xiaoyu Yang, Xiaoyun Yang, Xiaozhen Yang, Xifei Yang, Xiling Yang, Ximan Yang, Xin Yang, Xin-He Yang, Xin-Yu Yang, Xin-Zhuang Yang, Xing Yang, Xinghai Yang, Xinglong Yang, Xingmao Yang, Xingming Yang, Xingsheng Yang, Xingyu Yang, Xingyue Yang, Xingzhi Yang, Xinjing Yang, Xinming Yang, Xinpu Yang, Xinwang Yang, Xinxin Yang, Xinyan Yang, Xinyi Yang, Xinyu Yang, Xinyue Yang, Xiong Ling Yang, Xiru Yang, Xitong Yang, Xiu Hong Yang, Xiuhua Yang, Xiulin Yang, Xiuna Yang, Xiuqin Yang, Xiurong Yang, Xiuwei Yang, Xiwen Yang, Xiyue Yang, Xu Yang, Xuan Yang, Xue Yang, Xue-Feng Yang, Xue-Ping Yang, Xuecheng Yang, Xuehan Yang, Xuejing Yang, Xuejun Yang, Xueli Yang, Xuena Yang, Xueping Yang, Xuesong Yang, Xuhan Yang, Xuhui Yang, Xuping Yang, Xuyang Yang, Y C Yang, Y F Yang, Y L Yang, Y P Yang, Y Q Yang, Y Yang, Y-T Yang, Ya Yang, Ya-Chen Yang, Yadong Yang, Yafang Yang, Yajie Yang, Yalan Yang, Yali Yang, Yaming Yang, Yan Yang, Yan-Bei Yang, Yan-Ling Yang, Yanan Yang, Yanfang Yang, Yang Yang, Yangfan Yang, Yangyang Yang, Yanhui Yang, Yanjianxiong Yang, Yanling Yang, Yanmei Yang, Yanmin Yang, Yanping Yang, Yanru Yang, Yanting Yang, Yanyan Yang, Yanzhen Yang, Yaorui Yang, Yaping Yang, Yaqi Yang, Yaxi Yang, Ye Yang, Yefa Yang, Yefeng Yang, Yeqing Yang, Yexin Yang, Yi Yang, Yi-Chieh Yang, Yi-Fang Yang, Yi-Feng Yang, Yi-Liang Yang, Yi-Ping Yang, Yi-ning Yang, Yibing Yang, Yichen Yang, Yidong Yang, Yifan Yang, Yifang Yang, Yifei Yang, Yifeng Yang, Yihe Yang, Yijie Yang, Yilian Yang, Yimei Yang, Yimin Yang, Yiming Yang, Yimu Yang, Yin-Rong Yang, Yinfeng Yang, Ying Yang, Ying-Hua Yang, Ying-Ying Yang, Yingdi Yang, Yingjun Yang, Yingqing Yang, Yingrui Yang, Yingxia Yang, Yingyu Yang, Yinhua Yang, Yining Yang, Yinxi Yang, Yiping Yang, Yiting Yang, Yiyi Yang, Yiying Yang, Yong Yang, Yong-Yu Yang, Yongfeng Yang, Yongguang Yang, Yonghong Yang, Yonghui Yang, Yongjia Yang, Yongjie Yang, Yongkang Yang, Yongqiang Yang, Yongsan Yang, Yongxin Yang, Yongxing Yang, Yongzhong Yang, Yoon La Yang, Yoon Mee Yang, Youhua Yang, YoungSoon Yang, Yu Yang, Yu-Fan Yang, Yu-Feng Yang, Yu-Jie Yang, Yu-Shi Yang, Yu-Tao Yang, Yu-Ting Yang, Yuan Yang, Yuan-Han Yang, Yuan-Jian Yang, Yuanhao Yang, Yuanjin Yang, Yuanquan Yang, Yuanrong Yang, Yuanying Yang, Yuanzhang Yang, Yuanzhi Yang, Yuchen Yang, Yucheng Yang, Yue Yang, Yueh-Ning Yang, Yuejin Yang, Yuexiang Yang, Yueze Yang, Yufan Yang, Yuhan Yang, Yuhang Yang, Yuhua Yang, Yujie Yang, Yujing Yang, Yulin Yang, Yuling Yang, Yulong Yang, Yun Yang, YunKai Yang, Yunfan Yang, Yung-Li Yang, Yunhai Yang, Yunlong Yang, Yunmei Yang, Yunwen Yang, Yunyun Yang, Yunzhao Yang, Yupeng Yang, Yuqi Yang, Yuta Yang, Yutao Yang, Yuting Yang, Yutong Yang, Yuwei Yang, Yuxi Yang, Yuxing Yang, Yuxiu Yang, Yuyan Yang, Yuyao Yang, Yuying Yang, Z Yang, Zaibin Yang, Zaiming Yang, Zaiqing Yang, Zanhao Yang, Ze Yang, Zemin Yang, Zeng-Ming Yang, Zengqiang Yang, Zengqiao Yang, Zeyu Yang, Zhang Yang, Zhangping Yang, Zhanyi Yang, Zhao Yang, Zhao-Na Yang, Zhaojie Yang, Zhaoli Yang, Zhaoxin Yang, Zhaoyang Yang, Zhaoyi Yang, Zhehan Yang, Zheming Yang, Zhen Yang, Zheng Yang, Zheng-Fei Yang, Zheng-lin Yang, Zhenglin Yang, Zhengqian Yang, Zhengtao Yang, Zhenguo Yang, Zhengyan Yang, Zhengzheng Yang, Zhengzhong Yang, Zhenhua Yang, Zhenjun Yang, Zhenmei Yang, Zhenqi Yang, Zhenrong Yang, Zhenwei Yang, Zhenxing Yang, Zhenyun Yang, Zhenzhen Yang, Zheyu Yang, Zhi Yang, Zhi-Can Yang, Zhi-Hong Yang, Zhi-Jun Yang, Zhi-Min Yang, Zhi-Ming Yang, Zhi-Rui Yang, Zhibo Yang, Zhichao Yang, Zhifen Yang, Zhigang Yang, Zhihang Yang, Zhihong Yang, Zhikuan Yang, Zhikun Yang, Zhimin Yang, Zhiming Yang, Zhiqiang Yang, Zhitao Yang, Zhiwei Yang, Zhixin Yang, Zhiyan Yang, Zhiyong Yang, Zhiyou Yang, Zhiyuan Yang, Zhongan Yang, Zhongfang Yang, Zhonghua Yang, Zhonghui Yang, Zhongli Yang, Zhongshu Yang, Zhongzhou Yang, Zhou Yang, Zhuliang Yang, Zhuo Yang, Zhuoya Yang, Zhuoyu Yang, Zi F Yang, Zi Yang, Zi-Han Yang, Zi-Wei Yang, Zicong Yang, Zifeng Yang, Zihan Yang, Ziheng Yang, Zijiang Yang, Zishan Yang, Zixia Yang, Zixuan Yang, Ziying Yang, Ziyou Yang, Ziyu Yang, Zong-de Yang, Zongfang Yang, Zongyu Yang, Zunxian Yang, Zuozhen Yang
articles

Mutations in

Feng Zhao, Jun-Yi Zhu, Adam Richman +13 more · 2019 · Journal of the American Society of Nephrology : JASN · added 2026-04-24
Studies have identified mutations in >50 genes that can lead to monogenic steroid-resistant nephrotic syndrome (SRNS). The We identified We identified two compound-heterozygous Mutations in
no PDF DOI: 10.1681/ASN.2018080786
NUP160

17-Hydroxy Wortmannin Restores TRAIL's Response by Ameliorating Increased Beclin 1 Level and Autophagy Function in TRAIL-Resistant Colon Cancer Cells.

Sheng Dai, Shu Yang, Xin Hu +8 more · 2019 · Molecular cancer therapeutics · added 2026-04-24
Targeting of extrinsic apoptosis pathway by TNF-related apoptosis-inducing ligand (TRAIL) is an attractive approach for cancer therapy. However, two TRAIL drug candidates failed in clinical trials due Show more
Targeting of extrinsic apoptosis pathway by TNF-related apoptosis-inducing ligand (TRAIL) is an attractive approach for cancer therapy. However, two TRAIL drug candidates failed in clinical trials due to lack of efficacy. We identified 17-hydroxy wortmannin (17-HW) in a drug repurposing screen that resensitized TRAIL's response in the resistant colon cancer cells. The deficiency of caspase-8 in drug-resistant cells along with defects in apoptotic cell death was corrected by 17-HW, an inhibitor of PIK3C3-beclin 1 (BECN1) complex and autophagy activity. Further study found that BECN1 significantly increased in the TRAIL-resistant cells, resulting in increased autophagosome formation and enhanced autophagy flux. The extracellular domain (ECD) of BECN1 directly bound to the caspase-8 catalytic subunit (p10), leading to sequestration of caspase-8 in the autophagosome and its subsequent degradation. Inhibition of BECN1 restored the caspase-8 level and TRAIL's apoptotic response in the resistant colon cancer cells. An analysis of 120 colon cancer patient tissues revealed a correlation of a subgroup of patients (30.8%, 37/120) who have high BECN1 level and low caspase-8 level with a poor survival rate. Our study demonstrates that the increased BECN1 accompanied by enhanced autophagy activity is responsible for the TRAIL resistance, and a combination of TRAIL with a PIK3C3-BECN1 inhibitor is a promising therapeutic approach for the treatment of colon cancer. Show less
no PDF DOI: 10.1158/1535-7163.MCT-18-1241
PIK3C3

RNA-Binding Motif Protein 6 is a Candidate Serum Biomarker for Pancreatic Cancer.

Baojun Duan, Xiaoyan Hu, Meiyang Fan +9 more · 2019 · Proteomics. Clinical applications · Wiley · added 2026-04-24
Early diagnosis is crucial to improve outcomes for pancreatic cancer patients (PC). The present study is designed to identify differently expressed peptides involved in PC as potential biomarkers. The Show more
Early diagnosis is crucial to improve outcomes for pancreatic cancer patients (PC). The present study is designed to identify differently expressed peptides involved in PC as potential biomarkers. The serum proteome of 22 PC patients, 12 pancreatitis patients (PP), and 45 healthy controls (HC) are analyzed using magnetic bead-based weak cation exchange (MB-WCX) and matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS). Next, a supervised neural network (SNN) algorithm model is established by ClinProTools and the candidate biomarker identified using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS). Finally, the candidate biomarker is validated in tissue samples. The SNN algorithm model discriminates PC from HC with 92.97% sensitivity and 94.55% specificity. Seventy-six differentially expressed peptides are identified, seven of which are significantly different among PC, PP, and HC (p < 0.05). Only one peak (m/z: 1466.99) tends to be upregulated in samples from HC, PP, and PC, which is identified as region of RNA-binding motif protein 6 (RBM6). In subsequent tissue analysis, it is verified that RBM6 expression is significantly higher in PC tissues than paracancerous tissue. The results indicate that RBM6 might serve as a candidate diagnostic biomarker for PC. Methods used in this study could generate serum peptidome profiles of PC, PP, and HC, and present an approach to identify potential biomarkers for diagnosis of this malignancy. Show less
no PDF DOI: 10.1002/prca.201900048
RBM6

The long noncoding RNA LINC00483 promotes lung adenocarcinoma progression by sponging miR-204-3p.

Shengzhuang Yang, Tao Liu, Yu Sun +1 more · 2019 · Cellular & molecular biology letters · BioMed Central · added 2026-04-24
The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). However, its role in the progression of LUAD and the underlying mechanisms remain elusive. The expressi Show more
The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). However, its role in the progression of LUAD and the underlying mechanisms remain elusive. The expressions of LINC00483 and miR-204-3p were determined using quantitative real-time PCR. The correlation between the clinicopathological characteristics of LUAD patients and LINC00483 expression was analyzed using Pearson's χ LINC00483 was upregulated in LUAD tissues and cell lines. Higher LINC00483 levels closely correlated to shorter survival times, advanced TNM stage, larger tumor size and positive lymph node metastasis. Cell proliferation, migration and invasion were suppressed after LINC00483 knockdown. LINC00483 mainly localized in the cytoplasm, where it acted as a sponge of miR-204-3p. ETS1 was validated as a downstream target of miR-204-3p and is thus regulated by LINC00483. This study demonstrated that LINC00483 facilitates the proliferation, migration and invasion of LUAD cells by acting as a sponge for miR-204-3p, which in turn regulates ETS1. Show less
no PDF DOI: 10.1186/s11658-019-0192-7
SNAI1

[Semaphorin 6D and Snail are highly expressed in gastric cancer and positively correlated with malignant clinicopathological indexes].

Sixuan Qu, Zhaoli Yang, Hongdi Tao +4 more · 2019 · Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology · added 2026-04-24
Objective To investigate the expression of semaphorin 6D (SEMA6D) and Snail and their clinicopathological implications in gastric cancer. Methods 54 cases of gastric cancer tissues and 26 paracancerou Show more
Objective To investigate the expression of semaphorin 6D (SEMA6D) and Snail and their clinicopathological implications in gastric cancer. Methods 54 cases of gastric cancer tissues and 26 paracancerous gastric mucosa were collected for detecting the expression of SEMA6D and Snail by immunohistochemistry and Western blot analysis. The co-localization of SEMA6D and Snail was observed by immunofluorescence double staining and laser scanning confocal microscopy. The correlation between SEMA6D and Snail and their relationships with the clinicopathological features of the patients were analyzed. Results Compared with the paracancerous gastric mucosa, the protein expression of SEMA6D and Snail in the gastric cancer significantly increased, and there was a significant co-localization of SEMA6D and Snail in gastric cancer. Further statistical analysis showed that the expression of SEMA6D and Snail in gastric cancer was positively correlated with the degree of differentiation, invasion, lymph node metastasis and TNM stage. Conclusion The high expression of SEMA6D and Snail in gastric cancer are related to the malignant clinicopathological indexes of gastric cancer. Show less
no PDF
SNAI1

[Expression of β-catenin in Skin Lesions of Patients with Scleroderma and Its Effect on Epithelial-Mesenchymal Transition of Human Epidermal Keratinocytes].

Jin-Juan Liu, Hong-Fa Yang, Yong-Jian Li +1 more · 2019 · Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · added 2026-04-24
To investigate the expression of β-catenin in the skin lesions of patients with systemic scleroderma (SSc) and its effect on epithelial-mesenchymal transition (EMT) of human epidermal keratinocytes. T Show more
To investigate the expression of β-catenin in the skin lesions of patients with systemic scleroderma (SSc) and its effect on epithelial-mesenchymal transition (EMT) of human epidermal keratinocytes. The expression of β-catenin, Snail1 and E-cadherin in the skin lesions sample of 45 SSc patients and normal skin sample from 20 healthy adults was detected with SP immunohistochemistry. HaCaT, the human epidermal keratinocytes, were treated with different concentrations of Wnt10b (0 ng/mL (control), 2 ng/mL and 4 ng/mL) for 48 h. then detected the localization of β-catenin in HaCaT cells by immunofluorescence assay, determined the mRNA levels of Snail1 and Snail2 in HaCaT cells by real-time fluorescent quantitative PCR, detected the proteins expression of β-catenin, Vimentin, N-cadherin and E-cadherin in HaCaT cells by Western blot. The positive rates of β-catenin, Snail1 and E-cadherin in skin lesions of SSc patients were 100%, 88.89% and 2.22% respectively, while in healthy adult skin, the corresponding positive rates were 0%, 10.00%, and 95.00%. The difference between the two groups was significant. Compared with control group, treatment with different concentrations of Wnt10b (2 ng/mL and 4 ng/mL) induced up-regulation of β-catenin expression and promoted translocation of β-catenin from cytoplasm to nucleus, increased the mRNA levels of Snail1 and Snail2 ( Abnormally activated Wnt/β-catenin signaling pathway and abnormally expressed EMT-related proteins are observed in SSc lesions. Activation of Wnt/β-catenin signaling pathway may promote EMT in HaCaT cells. Show less
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SNAI1

Induced Pluripotent Stem Cells Attenuate Endothelial Leakage in Acute Lung Injury via Tissue Inhibitor of Metalloproteinases-1 to Reduce Focal Adhesion Kinase Activity.

Vincent Yi-Fong Su, Shih-Hwa Chiou, Chi-Shiuan Lin +2 more · 2019 · Stem cells (Dayton, Ohio) · Wiley · added 2026-04-24
Induced pluripotent stem cells (iPSCs) can reduce the severity of endotoxin-induced acute lung injury (ALI). However, the interaction between iPSCs and vascular endothelium remains unclear. In this st Show more
Induced pluripotent stem cells (iPSCs) can reduce the severity of endotoxin-induced acute lung injury (ALI). However, the interaction between iPSCs and vascular endothelium remains unclear. In this study, we investigated the effects of iPSCs in moderating pulmonary endothelial leakage in endotoxin-induced ALI. Murine iPSCs were delivered intravenously to male C57BL/6 mice (8-12 weeks old) 4 hours after intratracheal lipopolysaccharide (LPS) delivery. Histology, blood and bronchoalveolar lavage fluid (BALF) cytokine and junctional protein assays, and regulatory signaling pathway assays were performed 24 hours later. Human umbilical vein endothelial cells (HUVECs) were used as a model of junctional protein-expressing cells and stimulated with LPS. Our results showed that iPSC treatment alleviated histological signs of ALI, protein leakage, and proinflammatory cytokines. iPSC therapy restored vascular endothelial cadherin (VE-cadherin) expression in ALI mouse lungs. In HUVECs, human iPSCs (hiPSCs) restored disrupted VE-cadherin expression and reduced the activity of Snail and focal adhesion kinase (FAK) phosphorylation in Tyr397 in response to LPS. iPSC-conditioned medium contained extra antiangiogenic factor of tissue inhibitor of metalloproteinases-1 (TIMP-1) compared with control medium. TIMP-1 inhibition diminished the beneficial effects of iPSC-conditioned medium in ALI mice. Our study suggested that iPSCs attenuate endothelial cell leakage in endotoxin-induced ALI via a mechanism involving TIMP-1 and the FAK/Snail pathway. Stem Cells 2019;37:1516-1527. Show less
no PDF DOI: 10.1002/stem.3093
SNAI1

Antitumor activity of a novel dual functional podophyllotoxin derivative involved PI3K/AKT/mTOR pathway.

Yongli Li, Tengfei Huang, Yun Fu +6 more · 2019 · PloS one · PLOS · added 2026-04-24
The progression of cancer through local expansion and metastasis is well recognized, but preventing these characteristic cancer processes is challenging. To this end, a new strategy is required. In th Show more
The progression of cancer through local expansion and metastasis is well recognized, but preventing these characteristic cancer processes is challenging. To this end, a new strategy is required. In this study, we presented a novel dual functional podophyllotoxin derivative, 2-pyridinealdehyde hydrazone dithiocarbamate S-propionate podophyllotoxin ester (PtoxPdp), which inhibited both matrix metalloproteinases and Topoisomerase II. This new podophyllotoxin derivative exhibited significant anti-proliferative, anti-metastatic that correlated with the downregulation of matrix metalloproteinase. In a xenograft animal local expansion model, PtoxPdp was superior to etoposide in tumor repression. A preliminary mechanistic study revealed that PtoxPdp induced apoptosis and autophagy via the PI3K/AKT/mTOR pathway. Furthermore, PtoxPdp could also inhibit epithelial-mesenchymal transition, which was achieved by downregulating both PI3K/AKT/mTOR and NF-κB/Snail pathways. Taken together, our results reveal that PtoxPdp is a promising antitumor drug candidate. Show less
no PDF DOI: 10.1371/journal.pone.0215886
SNAI1

FAM83A signaling induces epithelial-mesenchymal transition by the PI3K/AKT/Snail pathway in NSCLC.

Fengrui Zhou, Jianxiong Geng, Shanqi Xu +6 more · 2019 · Aging · Impact Journals · added 2026-04-24
Family with sequence similarity 83, member A (FAM83A), as a potential tumor promoter, was reported to contribute to the progression of several malignant tumors. However, the significance of FAM83A in Show more
Family with sequence similarity 83, member A (FAM83A), as a potential tumor promoter, was reported to contribute to the progression of several malignant tumors. However, the significance of FAM83A in invasion and metastasis of non-small cell lung cancer (NSCLC) remains largely unknown. In this study, we found that FAM83A expression was significantly increased in NSCLC tissues. High expression of FAM83A was positively associated with tumor metastasis and poor survival of NSCLC patients. Functional experiments revealed that FAM83A knockdown could suppress NSCLC cell migration and invasion both Show less
no PDF DOI: 10.18632/aging.102163
SNAI1

Long noncoding RNA lnc-DILC stabilizes PTEN and suppresses clear cell renal cell carcinoma progression.

Han Zhang, Pengtao Wei, Wenwei Lv +3 more · 2019 · Cell & bioscience · BioMed Central · added 2026-04-24
Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are crucial regulators affecting the progression of human cancers. Recently, lncRNA downregulated in liver cancer stem cells (lnc-D Show more
Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are crucial regulators affecting the progression of human cancers. Recently, lncRNA downregulated in liver cancer stem cells (lnc-DILC) was identified to function as a tumor suppressor inhibiting the tumorigenesis and metastasis in liver cancer and colorectal cancer. However, to date, little is known about the functional roles of lnc-DILC in modulating malignant phenotypes of clear cell renal cell carcinoma (ccRCC) cells. lnc-DILC expression in human ccRCC tissues was detected by qRT-PCR. Overexpression and knockdown experiments were carried out to determine the effects of lnc-DILC on ccRCC cell proliferation, migration and invasion. To reveal the underlying mechanisms of lnc-DILC functions in ccRCC cells. RNA immunoprecipitation, RNA pull-down, in vivo ubiquitination, co-immunoprecipitation and western blot assays were performed. Here, we identified that lnc-DILC levels were dramatically downregulated in ccRCC tissues. Loss of lnc-DILC expression was correlated with larger tumor size, advanced tumor grade and lymph node metastasis, and also predicted worse prognosis in patients with ccRCC. Functionally, knockdown and overexpression experiments demonstrated that lnc-DILC inhibited cell proliferation, migration and invasion in ccRCC cells. Mechanistic investigation revealed that lnc-DILC bound to tumor suppressor PTEN and suppressed its degradation. lnc-DILC repressed the PTEN ubiquitination through blocking the interaction between PTEN and E3 ubiquitin ligase WWP2 and recruiting the deubiquitinase USP11 to PTEN. Moreover, we demonstrated that PTEN-AKT signaling was crucial for lnc-DILC-mediated suppressive effects. In summary, our research revealed a novel mechanism by which lnc-DILC regulates PTEN stability via WWP2 and USP11, and shed light on potential therapeutic strategies by the restoration of lnc-DILC expression in patients with ccRCC. Show less
no PDF DOI: 10.1186/s13578-019-0345-4
WWP2

Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma.

Meijuan Geng, Yiyi Yang, Xinyi Cao +3 more · 2019 · Biochemical and biophysical research communications · Elsevier · added 2026-04-24
Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer, with no effective treatment available. Identification of new anti-ATC drugs represents an urgent need. In this study, Show more
Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer, with no effective treatment available. Identification of new anti-ATC drugs represents an urgent need. In this study, we find that ATC cells are highly sensitive to THZ531, a potent inhibitor of the transcriptional cyclin-dependent kinase (CDK), CDK12. Cell-based assays demonstrate that CDK12 inhibition significantly impedes cell cycle progression, induces apoptotic cell death, and impairs colony formation in ATC cells. THZ531 causes a loss of elongating RNA polymerase II and suppresses gene expression in ATC cells. An integrative analysis of gene expression profiles and super-enhancer landscape, combining with functional assays, leads to the discovery of two new ATC cancer genes, ZC3H4 and NEMP1. Furthermore, CDK12 inhibition enhances the sensitivity of ATC cells to doxorubicin-mediated chemotherapy. Thus, these findings indicate that CDK12 is a potential therapeutic target for ATC treatment and its inhibition may help to overcome the chemoresistance in patients with ATC. Show less
no PDF DOI: 10.1016/j.bbrc.2019.10.052
ZC3H4

The emerging roles of a novel CCCH-type zinc finger protein, ZC3H4, in silica-induced epithelial to mesenchymal transition.

Rong Jiang, Zewei Zhou, Yan Liao +7 more · 2019 · Toxicology letters · Elsevier · added 2026-04-24
The epithelial to mesenchymal transition (EMT) contributes to fibrosis during silicosis. Zinc finger CCCH-type containing 4 protein (ZC3H4) is a novel CCCH-type zinc finger protein that activates infl Show more
The epithelial to mesenchymal transition (EMT) contributes to fibrosis during silicosis. Zinc finger CCCH-type containing 4 protein (ZC3H4) is a novel CCCH-type zinc finger protein that activates inflammation in pulmonary macrophages during silicosis. However, whether ZC3H4 is involved in EMT during silicosis remains unclear. In this study, we investigated the circular ZC3H4 (circZC3H4) RNA/microRNA-212 (miR-212) axis as the upstream molecular mechanism regulating ZC3H4 expression and the downstream mechanism by which ZC3H4 regulates EMT as well as its accompanying migratory characteristics. The protein levels were assessed via Western blotting and immunofluorescence staining. Scratch assays were used to analyze the increased mobility induced by silica. The CRISPR/Cas9 system and small interfering RNAs (siRNAs) were employed to analyze the regulatory mechanisms of ZC3H4 in EMT and migration changes. Specific knockdown of ZC3H4 blocked EMT and migration induced by silicon dioxide (SiO ZC3H4 may act as a novel regulator in the progression of SiO Show less
no PDF DOI: 10.1016/j.toxlet.2019.02.014
ZC3H4

Association between expression levels and growth trait-related SNPs located in promoters of the MC4R and MSTN genes in Spinibarbus hollandi.

Yang Yang, Zhaojun Lan, Hu Shu +4 more · 2018 · Genes & genomics · Springer · added 2026-04-24
Melanocortin 4 receptor: (MC4R) and Myostatin (MSTN) are two important growth trait-related genes in animals. In this study, we showed that two SNPs, MC4R-719A>G and MSTN-519C>T, found in the promoter Show more
Melanocortin 4 receptor: (MC4R) and Myostatin (MSTN) are two important growth trait-related genes in animals. In this study, we showed that two SNPs, MC4R-719A>G and MSTN-519C>T, found in the promoters of the MC4R and MSTN genes, respectively, are both associated with growth traits in Spinibarbus hollandi. Furthermore, we observed that there were significant associations between the expression levels of the MC4R and MSTN genes and these two growth trait-related SNPs. The expression level of MC4R gene in brain was lower in GG genotype fish with extremely high growth performance than that in AA genotype fish with extremely low growth performance. Expression level of the MSTN gene in muscle was lower in TT genotype fish with extremely high growth performance than that in CC and CT genotype fish with lower growth performance. The results indicated that these SNPs located in the promoters of MC4R and MSTN are associated with growth-related traits through modification of gene expression levels. The MSTN and MC4R SNPs may have useful application in effective marker-assisted selection aimed to increase output in S. hollandi. Show less
no PDF DOI: 10.1007/s13258-018-0666-4
MC4R

Melanocortin-4 receptor in subthalamic nucleus is involved in the modulation of nociception.

Dong-Ji Han, Zhi-Gang He, Hui Yang · 2018 · American journal of clinical and experimental immunology · added 2026-04-24
Deep brain stimulation of the subthalamic nucleus (STN-DBS) stimulation produces significant improvement of overall pain related to Parkinson disease; however, the mechanisms underlying analgesic effe Show more
Deep brain stimulation of the subthalamic nucleus (STN-DBS) stimulation produces significant improvement of overall pain related to Parkinson disease; however, the mechanisms underlying analgesic effects of STN-DBS are still unknown. This report describes direct neuroanatomical evidence for the central melanocortinergic-opioidergic circuits in the STN. We investigated melanocortin-4 receptor (MC4R) and mu-opioid receptor (MOR)-positive expression of the STN in MC4R-GFP transgenic mice using fluorescence immunohistochemical detection. Immunohistochemistry showed a large number of MC4R-GFP- and MOR-positive neurons within the STN region, and approximately 50% of MC4R-GFP-positive neurons coexpressed MOR. The results of this study showed direct neuroanatomical evidence for the central melanocortinergic-opioidergic signaling in the STN region. These findings contribute to the view of melanocortinergic-opioidergic circuits in the subthalamic nucleus as a reliable source of modulating of nociception with therapeutic potential for alleviating pain. Show less
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MC4R

Melanocortin Receptor 4 Signaling Regulates Vertebrate Limb Regeneration.

Mengshi Zhang, Youwei Chen, Hanqian Xu +7 more · 2018 · Developmental cell · Elsevier · added 2026-04-24
Melanocortin 4 receptor (Mc4r) plays a crucial role in the central control of energy homeostasis, but its role in peripheral organs has not been fully explored. We have investigated the roles of hypot Show more
Melanocortin 4 receptor (Mc4r) plays a crucial role in the central control of energy homeostasis, but its role in peripheral organs has not been fully explored. We have investigated the roles of hypothalamus-mediated energy metabolism during Xenopus limb regeneration. We report that hypothalamus injury inhibits Xenopus tadpole limb regeneration. By loss-of-function and gain-of-function studies, we show that Mc4r signaling is required for limb regeneration in regeneration-competent tadpoles and stimulates limb regeneration in later-stage regeneration-defective tadpoles. It regulates limb regeneration through modulating energy homeostasis and ROS production. Even more interestingly, our results demonstrate that Mc4r signaling is regulated by innervation and α-MSH substitutes for the effect of nerves in limb regeneration. Mc4r signaling is also required for mouse digit regeneration. Thus, our findings link vertebrate limb regeneration with Mc4r-mediated energy homeostasis and provide a new avenue for understanding Mc4r signaling in the peripheral organs. Show less
📄 PDF DOI: 10.1016/j.devcel.2018.07.021
MC4R

Melanocortin-4 receptor in swamp eel (Monopterus albus): Cloning, tissue distribution, and pharmacology.

Ti-Lin Yi, Li-Kun Yang, Guo-Liang Ruan +2 more · 2018 · Gene · Elsevier · added 2026-04-24
Melanocortin-4 receptor (MC4R) plays critical roles in the regulation of various physiological processes, such as energy homeostasis, reproduction and sexual function, cardiovascular function, and oth Show more
Melanocortin-4 receptor (MC4R) plays critical roles in the regulation of various physiological processes, such as energy homeostasis, reproduction and sexual function, cardiovascular function, and other functions in mammals. Although the functions of the MC4R in fish have not been extensively studied, the importance of MC4R in regulation of piscine energy expenditure and sexual functions is emerging. Swamp eel (Monopterus albus) is an economically and evolutionarily important fish widely distributed in tropics and subtropics. We cloned swamp eel mc4r (mamc4r), consisting of a 981 bp open reading frame encoding a protein of 326 amino acids. The sequence of maMC4R was homologous to those of several teleost MC4Rs. Phylogenetic and chromosomal synteny analyses showed that maMC4R was closely related to piscine MC4Rs. qRT-PCR revealed that mc4r transcripts were highly expressed in brain and gonads of swamp eel. The maMC4R was further demonstrated to be a functional receptor by pharmacological studies. Four agonists, α-melanocyte stimulating hormone (α-MSH), β-MSH, [Nle Show less
no PDF DOI: 10.1016/j.gene.2018.07.056
MC4R

Pharmacological Effects and Regulatory Mechanisms of Tobacco Smoking Effects on Food Intake and Weight Control.

Tongyuan Hu, Zhongli Yang, Ming D Li · 2018 · Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · Springer · added 2026-04-24
Beyond promoting smoking initiation and preventing smokers from quitting, nicotine can reduce food intake and body weight and thus is viewed as desirable by some smokers, especially many women. During Show more
Beyond promoting smoking initiation and preventing smokers from quitting, nicotine can reduce food intake and body weight and thus is viewed as desirable by some smokers, especially many women. During the last several decades, the molecular mechanisms underlying the inverse correlation between smoking and body weight have been investigated extensively in both animals and humans. Nicotine's weight effects appear to result especially from the drug's stimulation of α3β4 nicotine acetylcholine receptors (nAChRs), which are located on pro-opiomelanocortin (POMC) neurons in the arcuate nucleus (ARC), leading to activation of the melanocortin circuit, which is associated with body weight. Further, α7- and α4β2-containing nAChRs have been implicated in weight control by nicotine. This review summarizes current understanding of the regulatory effects of nicotine on food intake and body weight according to the findings from pharmacological, molecular genetic, electrophysiological, and feeding studies on these appetite-regulating molecules, such as α3β4, α7, and α4β2 nAChRs; neuropeptide Y (NPY); POMC; melanocortin 4 receptor (MC4R); agouti-related peptide (AgRP); leptin, ghrelin, and protein YY (PYY). Show less
no PDF DOI: 10.1007/s11481-018-9800-y
MC4R

Melanocortin 4 Receptor Pathway Dysfunction in Obesity: Patient Stratification Aimed at MC4R Agonist Treatment.

Kristin L Ayers, Benjamin S Glicksberg, Alastair S Garfield +15 more · 2018 · The Journal of clinical endocrinology and metabolism · added 2026-04-24
The hypothalamic melanocortin 4 receptor (MC4R) pathway serves a critical role in regulating body weight. Loss of function (LoF) mutations in the MC4R pathway, including mutations in the pro-opiomelan Show more
The hypothalamic melanocortin 4 receptor (MC4R) pathway serves a critical role in regulating body weight. Loss of function (LoF) mutations in the MC4R pathway, including mutations in the pro-opiomelanocortin (POMC), prohormone convertase 1 (PCSK1), leptin receptor (LEPR), or MC4R genes, have been shown to cause early-onset severe obesity. Through a comprehensive epidemiological analysis of known and predicted LoF variants in the POMC, PCSK1, and LEPR genes, we sought to estimate the number of US individuals with biallelic MC4R pathway LoF variants. We predict ~650 α-melanocyte-stimulating hormone (MSH)/POMC, 8500 PCSK1, and 3600 LEPR homozygous and compound heterozygous individuals in the United States, cumulatively enumerating >12,800 MC4R pathway-deficient obese patients. Few of these variants have been genetically diagnosed to date. These estimates increase when we include a small subset of less rare variants: β-MSH/POMC,PCSK1 N221D, and a PCSK1 LoF variant (T640A). To further define the MC4R pathway and its potential impact on obesity, we tested associations between body mass index (BMI) and LoF mutation burden in the POMC, PCSK1, and LEPR genes in various populations. We show that the cumulative allele burden in individuals with two or more LoF alleles in one or more genes in the MC4R pathway are predisposed to a higher BMI than noncarriers or heterozygous LoF carriers with a defect in only one gene. Our analysis represents a genetically rationalized study of the hypothalamic MC4R pathway aimed at genetic patient stratification to determine which obese subpopulations should be studied to elucidate MC4R agonist (e.g., setmelanotide) treatment responsiveness. Show less
📄 PDF DOI: 10.1210/jc.2018-00258
MC4R

Variants in genes encoding small GTPases and association with epithelial ovarian cancer susceptibility.

Madalene Earp, Jonathan P Tyrer, Stacey J Winham +146 more · 2018 · PloS one · PLOS · added 2026-04-24
Madalene Earp, Jonathan P Tyrer, Stacey J Winham, Hui-Yi Lin, Ganna Chornokur, Joe Dennis, Katja K H Aben, Hoda Anton-Culver, Natalia Antonenkova, Elisa V Bandera, Yukie T Bean, Matthias W Beckmann, Line Bjorge, Natalia Bogdanova, Louise A Brinton, Angela Brooks-Wilson, Fiona Bruinsma, Clareann H Bunker, Ralf Butzow, Ian G Campbell, Karen Carty, Jenny Chang-Claude, Linda S Cook, Daniel W Cramer, Julie M Cunningham, Cezary Cybulski, Agnieszka Dansonka-Mieszkowska, Evelyn Despierre, Jennifer A Doherty, Thilo Dörk, Andreas du Bois, Matthias Dürst, Douglas F Easton, Diana M Eccles, Robert P Edwards, Arif B Ekici, Peter A Fasching, Brooke L Fridley, Aleksandra Gentry-Maharaj, Graham G Giles, Rosalind Glasspool, Marc T Goodman, Jacek Gronwald, Philipp Harter, Alexander Hein, Florian Heitz, Michelle A T Hildebrandt, Peter Hillemanns, Claus K Hogdall, Estrid Høgdall, Satoyo Hosono, Edwin S Iversen, Anna Jakubowska, Allan Jensen, Bu-Tian Ji, Audrey Y Jung, Beth Y Karlan, Melissa Kellar, Lambertus A Kiemeney, Boon Kiong Lim, Susanne K Kjaer, Camilla Krakstad, Jolanta Kupryjanczyk, Diether Lambrechts, Sandrina Lambrechts, Nhu D Le, Shashi Lele, Jenny Lester, Douglas A Levine, Zheng Li, Dong Liang, Jolanta Lissowska, Karen Lu, Jan Lubinski, Lene Lundvall, Leon F A G Massuger, Keitaro Matsuo, Valerie McGuire, John R McLaughlin, Iain McNeish, Usha Menon, Roger L Milne, Francesmary Modugno, Kirsten B Moysich, Roberta B Ness, Heli Nevanlinna, Kunle Odunsi, Sara H Olson, Irene Orlow, Sandra Orsulic, James Paul, Tanja Pejovic, Liisa M Pelttari, Jenny B Permuth, Malcolm C Pike, Elizabeth M Poole, Barry Rosen, Mary Anne Rossing, Joseph H Rothstein, Ingo B Runnebaum, Iwona K Rzepecka, Eva Schernhammer, Ira Schwaab, Xiao-Ou Shu, Yurii B Shvetsov, Nadeem Siddiqui, Weiva Sieh, Honglin Song, Melissa C Southey, Beata Spiewankiewicz, Lara Sucheston-Campbell, Ingvild L Tangen, Soo-Hwang Teo, Kathryn L Terry, Pamela J Thompson, Lotte Thomsen, Shelley S Tworoger, Anne M van Altena, Ignace Vergote, Liv Cecilie Vestrheim Thomsen, Robert A Vierkant, Christine S Walsh, Shan Wang-Gohrke, Nicolas Wentzensen, Alice S Whittemore, Kristine G Wicklund, Lynne R Wilkens, Yin-Ling Woo, Anna H Wu, Xifeng Wu, Yong-Bing Xiang, Hannah Yang, Wei Zheng, Argyrios Ziogas, Alice W Lee, Celeste L Pearce, Andrew Berchuck, Joellen M Schildkraut, Susan J Ramus, Alvaro N A Monteiro, Steven A Narod, Thomas A Sellers, Simon A Gayther, Linda E Kelemen, Georgia Chenevix-Trench, Harvey A Risch, Paul D P Pharoah, Ellen L Goode, Catherine M Phelan Show less
Epithelial ovarian cancer (EOC) is the fifth leading cause of cancer mortality in American women. Normal ovarian physiology is intricately connected to small GTP binding proteins of the Ras superfamil Show more
Epithelial ovarian cancer (EOC) is the fifth leading cause of cancer mortality in American women. Normal ovarian physiology is intricately connected to small GTP binding proteins of the Ras superfamily (Ras, Rho, Rab, Arf, and Ran) which govern processes such as signal transduction, cell proliferation, cell motility, and vesicle transport. We hypothesized that common germline variation in genes encoding small GTPases is associated with EOC risk. We investigated 322 variants in 88 small GTPase genes in germline DNA of 18,736 EOC patients and 26,138 controls of European ancestry using a custom genotype array and logistic regression fitting log-additive models. Functional annotation was used to identify biofeatures and expression quantitative trait loci that intersect with risk variants. One variant, ARHGEF10L (Rho guanine nucleotide exchange factor 10 like) rs2256787, was associated with increased endometrioid EOC risk (OR = 1.33, p = 4.46 x 10-6). Other variants of interest included another in ARHGEF10L, rs10788679, which was associated with invasive serous EOC risk (OR = 1.07, p = 0.00026) and two variants in AKAP6 (A-kinase anchoring protein 6) which were associated with risk of invasive EOC (rs1955513, OR = 0.90, p = 0.00033; rs927062, OR = 0.94, p = 0.00059). Functional annotation revealed that the two ARHGEF10L variants were located in super-enhancer regions and that AKAP6 rs927062 was associated with expression of GTPase gene ARHGAP5 (Rho GTPase activating protein 5). Inherited variants in ARHGEF10L and AKAP6, with potential transcriptional regulatory function and association with EOC risk, warrant investigation in independent EOC study populations. Show less
📄 PDF DOI: 10.1371/journal.pone.0197561
AKAP6

Gut Microbiota Is a Major Contributor to Adiposity in Pigs.

Hua Yang, Yun Xiang, Kelsy Robinson +4 more · 2018 · Frontiers in microbiology · Frontiers · added 2026-04-24
Different breeds of pigs vary greatly in their propensity for adiposity. Gut microbiota is known to play an important role in modulating host physiology including fat metabolism. However, the relative Show more
Different breeds of pigs vary greatly in their propensity for adiposity. Gut microbiota is known to play an important role in modulating host physiology including fat metabolism. However, the relative contribution of gut microbiota to lipogenic characteristics of pigs remains elusive. In this study, we transplanted fecal microbiota of adult Jinhua and Landrace pigs, two breeds of pigs with distinct lipogenic phenotypes, to antibiotic-treated mice. Our results indicated that, 4 weeks after fecal transplantation, the mice receiving Jinhua pigs' "obese" microbiota (JM) exhibited a different intestinal bacterial community structure from those receiving Landrace pigs' "lean" microbiota (LM). Notably, an elevated ratio of Firmicutes to Bacteroidetes and a significant diminishment of Show less
📄 PDF DOI: 10.3389/fmicb.2018.03045
ANGPTL4

Preventive effect of Tongxinluo on endothelial survival and vascular integrity, together with inhibition of inflammatory reaction in rats model of intestine ischemia/reperfusion injury.

Jun-Xiu Zhang, Shao-Dan Li, Yi Liu +1 more · 2018 · Pakistan journal of pharmaceutical sciences · added 2026-04-24
This study was design to investigate preventive function of Tongxinluo (TXL) capsule on micro vascular function and endothelial survival in rats model of intestine ischemia/reperfusion (I/R) injury. W Show more
This study was design to investigate preventive function of Tongxinluo (TXL) capsule on micro vascular function and endothelial survival in rats model of intestine ischemia/reperfusion (I/R) injury. We randomly divided fifty male Sprague-Dawley rats into Sham group, I/R group, TXL0.4+I/R group, TXL0.8+I/R group, TXL1.6+I/R group (10 rats each). Rat intestine I/R injury was carried out using a model of acute superior mesenteric artery occlusion with 30 min ischemia followed by 60 min reperfusion. The distribution of endothelial apoptosis in intestine was determined by CD31+TUNEL immunofluorescent double staining analysis. VE-Cadherin, ANGPTL4, HMGB1 and NF-κB were determined by immunohistochemical analysis. I/R induced massively endothelial cell apoptosis, accompanied with reduced expression of adherens junction protein VE-Cadherin and up regulation of inflammatory mediator HMGB1 and NF-κB. TXL pretreatment groups (TXL0.4+I/R, TXL0.8+I/R and TXL1.6+I/R group) significantly attenuated endothelial cell apoptosis with a dose-dependent effect. TXL pretreatment could maintain the expression of VE-Cadherin and promote the expression of ANGPTL4 which help to maintain endothelial integrity. TXL pretreatment also exert great influence in inhibiting HMGB1 expression and NF-κB expression induced by I/R. It could be concluded from this study that micro vascular dysfunction and endothelial damage play a causal role in rat intestine I/R injury. TXL pretreatment could significantly prevent the I/R induced pathology of endothelial apoptosis, micro vascular integrity disruption and inflammatory reaction. Show less
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ANGPTL4

Sonic hedgehog promotes endothelial differentiation of bone marrow mesenchymal stem cells via VEGF-D.

Sheng Shi, Jiacheng Sun, Qingyou Meng +7 more · 2018 · Journal of thoracic disease · added 2026-04-24
Bone marrow-derived mesenchymal stem cells (BMSCs) have been proved to be capable of differentiating into endothelial cells (ECs), however, the differentiation efficiency is rather low. Sonic hedgehog Show more
Bone marrow-derived mesenchymal stem cells (BMSCs) have been proved to be capable of differentiating into endothelial cells (ECs), however, the differentiation efficiency is rather low. Sonic hedgehog (Shh), an important factor in vascular development and postnatal angiogenesis, exerted promotional effect on new vessel formation in the ischemic animal models. Therefore, the current study aims to investigate whether Shh could induce the endothelial differentiation of BMSCs both The current study over-expressed Shh in BMSCs by lentivirus transduction. Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) analysis was performed to determine the angiogenic factors in both control BMSCs and Shh over-expressed BMSCs. Immunocytochemistry was also conducted to examine the EC markers. Angiogenesis was determined by Shh expression was increased by about 3,000-fold and 5,000-fold at 3 days-transfection and 7 days-transfection, respectively. Patched 1 (Ptch1), the receptor for Shh, had a two-fold increase after transduction. The angiogenic factors such as hepatocyte growth factor (HGF), angiopoietin-1 (Ang-1), insulin-like growth factor 1 (IGF1) and vascular endothelial growth factor A (VEGF-A) had at least a 1.5-fold increase after transduction. Expression of EC-lineage markers, CD31 and VE-cadherin, on Shh-overexpressed BMSCs were increasingly detected by immunocytostaining. Angiogenesis of BMSCs could be efficiently induced by Shh overexpression in the This study demonstrated that Shh could promote endothelial differentiation of BMSCs via VEGF-D. Show less
no PDF DOI: 10.21037/jtd.2018.09.50
ANGPTL4

Long Non-coding RNA PVT1 Promotes Cell Proliferation and Migration by Silencing ANGPTL4 Expression in Cholangiocarcinoma.

Yang Yu, Mingjiong Zhang, Jie Liu +9 more · 2018 · Molecular therapy. Nucleic acids · Elsevier · added 2026-04-24
Cholangiocarcinoma (CCA) is the most common biliary tract malignancy, with a low survival rate and limited treatment options. Long non-coding RNAs (lncRNAs) have recently been verified to have signifi Show more
Cholangiocarcinoma (CCA) is the most common biliary tract malignancy, with a low survival rate and limited treatment options. Long non-coding RNAs (lncRNAs) have recently been verified to have significant regulatory functions in many kinds of human cancers. It was discovered in this study that the lncRNA PVT1, whose expression is significantly elevated in CCA, could be a molecular marker of CCA. Experiments indicated that PVT1 knockdown greatly inhibited cell migration and proliferation in vitro and in vivo. According to RNA sequencing (RNA-seq) analysis, PVT1 knockdown dramatically influenced target genes associated with cell angiogenesis, cell proliferation, and the apoptotic process. RNA immunoprecipitation (RIP) analysis demonstrated that, by binding to epigenetic modification complexes (PRC2), PVT1 could adjust the histone methylation of the promoter of ANGPTL4 (angiopoietin-like 4) and, thus, promote cell growth, migration, and apoptosis progression. The data verified the significant functions of PVT1 in CCA oncogenesis, and they suggested that PVT1 could be a target for CCA intervention. Show less
📄 PDF DOI: 10.1016/j.omtn.2018.10.001
ANGPTL4

ANGPTL4 variants and their haplotypes are associated with serum lipid levels, the risk of coronary artery disease and ischemic stroke and atorvastatin cholesterol-lowering responses.

Qian Yang, Rui-Xing Yin, Xiao-Li Cao +3 more · 2018 · Nutrition & metabolism · BioMed Central · added 2026-04-24
This study aimed to assess the association between the angiopoietin-like protein 4 gene ( Genotypes of the The rs2967605 CT/TT genotypes were associated with a decreased risk of CAD (adjusted OR = 0.6 Show more
This study aimed to assess the association between the angiopoietin-like protein 4 gene ( Genotypes of the The rs2967605 CT/TT genotypes were associated with a decreased risk of CAD (adjusted OR = 0.68, 95% CI = 0.47-0.99, The observed associations suggest that the Show less
📄 PDF DOI: 10.1186/s12986-018-0308-5
ANGPTL4

Response to comment by Guerra et al.

Xinyue Yang, Yan Cheng, Guanfang Su · 2018 · Bioscience reports · added 2026-04-24
This is a response by the authors of the review article 'A review of the multifunctionality of angiopoietin-like 4 in eye disease' [
📄 PDF DOI: 10.1042/BSR20181493
ANGPTL4

ANGPTL4 participates in gestational diabetes mellitus via regulating Akt pathway.

M Li, X-J Yang, G-Y Zhang +3 more · 2018 · European review for medical and pharmacological sciences · added 2026-04-24
To explore ANGPTL4 expressions in patients with gestational diabetes mellitus (GDM) and its underlying mechanism. We first detected serum expressions of ANGPTL4 in GDM patients and healthy pregnancies Show more
To explore ANGPTL4 expressions in patients with gestational diabetes mellitus (GDM) and its underlying mechanism. We first detected serum expressions of ANGPTL4 in GDM patients and healthy pregnancies. Subsequently, effects of ANGPTL4 knockdown on apoptosis, proliferation, and cell cycle in 3T3-L1 cells were determined, respectively. Effects of ANGPTL4 on glucose uptake and adipocyte differentiation were also evaluated, respectively. The cytokine secretion in adipocytes transfected with sh-ANGPTL4 was detected by quantitative Reverse Transcriptase-Polymerase Chain Reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Furthermore, effects of ANGPTL4 knockdown on NF-kB and Akt pathway were detected by Western blot. ANGPTL4 was down-regulated in serum of GDM patients. In vitro experiments suggested that down-regulated ANGPTL4 inhibited apoptosis and promoted proliferation of 3T3-L1 cells. Meanwhile, down-regulated ANGPTL4 significantly inhibited glucose uptake and Akt pathway. However, ANGPTL4 expression did not affect cell cycle and adipocyte differentiation. Detection of inflammatory cytokines suggested that down-regulated ANGPTL4 resulted in increased expressions of inflammatory cytokines and activation of NF-kB pathway. ANGPTL4 is down-regulated in GDM and may participate in the GDM development by promoting insulin resistance and secretion of inflammatory cytokines. Show less
no PDF DOI: 10.26355/eurrev_201808_15697
ANGPTL4

A review of the multifunctionality of angiopoietin-like 4 in eye disease.

Xinyue Yang, Yan Cheng, Guanfang Su · 2018 · Bioscience reports · added 2026-04-24
Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional cytokine regulating vascular permeability, angiogenesis, and inflammation. Dysregulations in these responses contribute to the pathogenesis o Show more
Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional cytokine regulating vascular permeability, angiogenesis, and inflammation. Dysregulations in these responses contribute to the pathogenesis of ischemic retinopathies such as diabetic retinopathy (DR), age-related macular degeneration (AMD), retinal vein occlusion, and sickle cell retinopathy (SCR). However, the role of ANGPTL4 in these diseases remains controversial. Here, we summarize the functional mechanisms of ANGPTL4 in several diseases. We highlight original studies that provide detailed data about the mechanisms of action for ANGPTL4, its applications as a diagnostic or prognostic biomarker, and its use as a potential therapeutic target. Taken together, the discussions in this review will help us gain a better understanding of the molecular mechanisms by which ANGPTL4 functions in eye disease and will provide directions for future research. Show less
📄 PDF DOI: 10.1042/BSR20180557
ANGPTL4

Differentiated adipose-derived stem cell cocultures for bone regeneration in RADA16-I in vitro.

Huifang Yang, Nanrui Hong, Hsiaowei Liu +3 more · 2018 · Journal of cellular physiology · Wiley · added 2026-04-24
Craniofacial defects can cause morbidness. Adipose-derived stem cells (ADSCs) have shown great promise for osteogeneration and vascularization; therefore cocultures of differentiated ADSCs are explore Show more
Craniofacial defects can cause morbidness. Adipose-derived stem cells (ADSCs) have shown great promise for osteogeneration and vascularization; therefore cocultures of differentiated ADSCs are explored to increase bone and vessel formation. In this study, ADSCs were induced into osteogenic ADSCs (os-ADSCs) and endothelial ADSCs (endo-ADSCs) cells, which were then cocultured in variable proportions (os-ADSCs/endo-ADSCs = 2:1, 1:1, 1:2). The os-ADSCs in a ratio of 1:1 expressed more ALP, RUNX2 and COL-I, whereas VEGF, vWF and CD31 were upregulated in the endo-ADSCs of this group. Next generation RNA sequencing (RNA-seq) was performed to evaluate the molecular mechanisms of cocultured ADSCs. The os-ADSCs and endo-ADSCs interacted with each other during osteogenic and angiogenic differentiation, especially at the ratio of 1:1, and were regulated by vascular-related genes, cell-mediated genes, bone-related genes and the transforming growth factor β signaling pathway (TGF-β), mitogen-activated protein kinase signaling pathway (MAPK) and wnt signaling pathway (Wnt). Angptl4, apoe, mmp3, bmp6, mmp13 and fgf18 were detected to be up-regulated, and cxcl12 and wnt5a were down-regulated. The results showed that the gene expression levels were consistent with that in RNA-seq. The cells were then seeded into self-assembling peptide RADA16-I scaffolds as cocultures (1:1) and monocultures (ADSCs, os-ADSCs, endo-ADSCs). The results showed that the cells of all groups grew and proliferated well on the scaffolds, and the cocultured group exhibited better osteogeneration and vascularization. In conclusion, cocultured os-ADSCs and endo-ADSCs at the ratio of 1:1 showed strong osteogenic and angiogenic differentiation. There is a great potential for osteogenesis and vascularization by 3D culturing cells in a 1:1 ratio in self-assembling peptide RADA16-I scaffolds, which requires evaluation for bone regeneration in vivo. Show less
no PDF DOI: 10.1002/jcp.26838
ANGPTL4

Tongxinluo attenuates reperfusion injury in diabetic hearts by angiopoietin-like 4-mediated protection of endothelial barrier integrity via PPAR-α pathway.

Kang Qi, Xiangdong Li, Yongjian Geng +5 more · 2018 · PloS one · PLOS · added 2026-04-24
Endothelial barrier function in the onset and Tongxinluo (TXL) protection of myocardial ischemia/reperfusion (I/R) injury, and TXL can induce the secretion of Angiopoietin-like 4 (Angptl4) in human ca Show more
Endothelial barrier function in the onset and Tongxinluo (TXL) protection of myocardial ischemia/reperfusion (I/R) injury, and TXL can induce the secretion of Angiopoietin-like 4 (Angptl4) in human cardiac microvascular endothelial cells during hypoxia/reoxygenation. We intend to demonstrate whether TXL can attenuate myocardial I/R injury in diabetes, characterized with microvascular endothelial barrier disruption, by induction of Angptl4-mediated protection of endothelial barrier integrity. I/R injury was created by coronary ligation in ZDF diabetic and non-diabetic control rats. The animals were anesthetized and randomized to sham operation or I/R injury with or without the exposure to insulin, rhAngptl4, TXL, Angptl4 siRNA, and the PPAR-α inhibitor MK886. Tongxinluo, insulin and rhAngptl4 have the similar protective effect on diabetic hearts against I/R injury. In I/R-injured diabetic hearts, TXL treatment remarkably reduced the infarct size, and protected endothelial barrier integrity demonstrated by decreased endothelial cells apoptosis, microvascular permeability, and myocardial hemorrhage, fortified tight junction, and upregulated expression of JAM-A, integrin-α5, and VE-cadherin, and these effects of TXL were as effective as insulin and rhAngptl4. However, Angptl4 knock-down with siRNA interference and inhibition of PPAR-α with MK886 partially diminished these beneficial effects of TXL and rhAngptl4. TXL induced the expression of Angptl4 in I/R-injured diabetic hearts, and was canceled by Angptl4 siRNA and MK886. TXL treatment increased myocardial PPAR-α activity, and was abolished by MK886 but not by Angptl4 siRNA. TXL protects diabetic hearts against I/R injury by activating Angptl4-mediated restoration of endothelial barrier integrity via the PPAR-α pathway. Show less
📄 PDF DOI: 10.1371/journal.pone.0198403
ANGPTL4

Angiopoietin-like 3 Is a Potential Biomarker for Retinopathy in Type 2 Diabetic Patients.

Cai-Guo Yu, Sha-Sha Yuan, Long-Yan Yang +7 more · 2018 · American journal of ophthalmology · Elsevier · added 2026-04-24
To investigate whether angiopoietin-like 3 (ANGPTL3) and angiopoietin-like 4 (ANGPTL4) are differentially associated with the severity of retinopathy in patients with type 2 diabetes mellitus (T2DM). Show more
To investigate whether angiopoietin-like 3 (ANGPTL3) and angiopoietin-like 4 (ANGPTL4) are differentially associated with the severity of retinopathy in patients with type 2 diabetes mellitus (T2DM). Cross-sectional study. Serum levels of ANGPTL3, ANGPTL4, high-sensitivity C-reactive protein (CRP), vascular adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), and vascular endothelial growth factor (VEGF) were quantified by ELISA. Retinal images were recorded to assess the grade of diabetic retinopathy (DR). Multivariable-adjusted logistic analysis was performed to estimate the association of each biomarker and DR stage. Among 1192 T2DM patients, 426 (35.7%) had nonproliferative diabetic retinopathy (NPDR) and 56 (4.5%) had proliferative diabetic retinopathy (PDR). After adjusting for covariables, the odds ratios expressing the risk of having DR vs no DR (n = 710 vs 482) were 1.23 (95% confidence interval [CI], 1.08-1.40, P = .002) for ANGPTL3; 0.90 (95% CI, 0.79-1.02; P = .095) for ANGPTL4; and 1.14 (95% CI, 1.00-1.29; P = .044) for VEGF. The risk of having no DR vs NPDR (n = 710 vs 426) was 1.16 (95% CI, 1.01-1.32; P = .036) for ANGPTL3; 0.90 (95% CI, 0.79-1.04; P = .15) for ANGPTL4; and 1.14 (95% CI, 1.00-1.31; P = .045) for VEGF. The odds ratios of having NPDR vs PDR (n = 426 vs 56) was 1.47 (95% CI, 1.03-2.10; P = .035) for serum ANGPTL3; 0.96 (95% CI, 0.69-1.35; P = .83) for ANGPTL4; and 1.05 (95% CI, 0.77-1.45; P = .74) for VEGF. ANGPTL3 is independently and strongly associated with DR progression in all stages. Blockade of ANGPTL3 signal in retina might postpone the onset and development of DR in T2DM patients. Show less
no PDF DOI: 10.1016/j.ajo.2018.03.040
ANGPTL4