Protection from renal fibrosis, putative role of TRIB3 gene silencing

被引:9
作者
Ding, Wen-yuan [1 ,2 ,3 ]
Li, Wen-bo [1 ,2 ,3 ]
Ti, Yun [1 ,2 ,3 ]
Bi, Xiu-ping [1 ,2 ,3 ]
Sun, Hui [1 ,2 ,3 ]
Wang, Zhi-hao [1 ,2 ,4 ]
Zhang, Yun [1 ,2 ,3 ]
Zhang, Wei [1 ,2 ,3 ]
Zhong, Ming [1 ,2 ,3 ]
机构
[1] Shandong Univ, Qilu Hosp, Chinese Minist Educ, Key Lab Cardiovasc Remodeling & Funct Res, Jinan 250012, Peoples R China
[2] Shandong Univ, Qilu Hosp, Chinese Minist Publ Hlth, Dept Cardiol, Jinan 250012, Peoples R China
[3] Shandong Univ, Qilu Hosp, Dept Cardiol, Jinan 250012, Peoples R China
[4] Shandong Univ, Qilu Hosp, Jinan 250012, Peoples R China
基金
中国国家自然科学基金;
关键词
TRIB3; siRNA; MAPK; Renal fibrosis; INSULIN-RESISTANCE; TRIBBLES HOMOLOG; INSIGHTS; TRB3; INHIBITION; ACTIVATION; DIET;
D O I
10.1016/j.yexmp.2013.12.003
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Background: Renal fibrosis is thought to be the common pathway in most cases of chronic kidney disease. Recently, TRIB3 was found to play an important role in progression of cardiac fibrosis in an insulin-resistant state. We investigated whether TRIB3 might participate in the pathogenesis of renal fibrosis in insulin-resistant rats. Methods: We randomly separated 40 male Sprague-Dawley into 4 groups for treatment (n = 10 each): control and high-fat diet (HFD) with TRIB3 siRNA adenovirus transfection, vehicle transfection or HFD alone. Insulin resistance markers were measured. Renal tissues were stained with hematoxylin and eosin, Masson's trichrome and periodic acid-Schiff. Results: Rats with HFD showed insulin resistance and TRIB3 overexpression. Upregulated TRIB3 expression could induce renal fibrosis accompanied by increased phosphorylation of extracellular signal-regulated kinase (ERK). Also, TRIB3 siRNA knockdown could ameliorate renal fibrosis, which was accompanied by decreased phosphorylation of ERK. Conclusions: TRIB3 gene silencing can attenuate renal fibrosis for beneficial effect on the development of renal fibrosis in chronic kidney disease in rat. Crown Copyright (C) 2014 Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:80 / 84
页数:5
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