期刊
EXPERIMENTAL AND MOLECULAR PATHOLOGY
卷 96, 期 1, 页码 80-84出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yexmp.2013.12.003
关键词
TRIB3; siRNA; MAPK; Renal fibrosis
类别
资金
- Key Technologies Research and Development Program of Shandong Province [2006GG2202020, 2010G0020262]
- Natural Science Foundation of Shandong Province [Y2005C11, ZR2009CM022, ZR2009CM025, BS2009YY026]
- National Natural Science Foundation of China [30871038, 30971215, 81070192, 81070141, 81100605, 81270287, 81270352]
- National Basic Research Program of China (973 Program) [2012CB722406]
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.
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