4.5 Article

Protection from renal fibrosis, putative role of TRIB3 gene silencing

Journal

EXPERIMENTAL AND MOLECULAR PATHOLOGY
Volume 96, Issue 1, Pages 80-84

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yexmp.2013.12.003

Keywords

TRIB3; siRNA; MAPK; Renal fibrosis

Categories

Funding

  1. Key Technologies Research and Development Program of Shandong Province [2006GG2202020, 2010G0020262]
  2. Natural Science Foundation of Shandong Province [Y2005C11, ZR2009CM022, ZR2009CM025, BS2009YY026]
  3. National Natural Science Foundation of China [30871038, 30971215, 81070192, 81070141, 81100605, 81270287, 81270352]
  4. National Basic Research Program of China (973 Program) [2012CB722406]

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.5
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available