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Journal of Immunology Research
Volume 2014 (2014), Article ID 240396, 11 pages
Research Article

Tribbles 3 Regulates the Fibrosis Cytokine TGF-β1 through ERK1/2-MAPK Signaling Pathway in Diabetic Nephropathy

1Department of Hemodialysis, Qilu Hospital, Shandong University, Jinan 250012, China
2General Department, Qilu Hospital, Shandong University, Jinan 250012, China

Received 18 March 2014; Revised 21 May 2014; Accepted 3 June 2014; Published 16 July 2014

Academic Editor: Joseph Fomusi Ndisang

Copyright © 2014 Luwei Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To reveal the expression and possible role of tribbles homolog 3 (TRB3) in the incidence of type 2 diabetic nephropathy, we used immunohistochemistry, real-time quantitative PCR, western blot analysis, and enzyme-linked immunosorbent assay (ELISA) to study the expression of TRB3, extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (ERK1/2 MAPK), transforming growth factor β1 (TGF-β1), and collagen type IV in kidneys of db/db diabetic mice and in murine renal mesangial cells stimulated with high glucose. The expression of TRB3, TGF-β1, and collagen type IV was increased in kidneys of db/db diabetic mice. TGF-β1 and collagen type IV regulated by high glucose through ERK1/2 MAPK were downregulated by silencing TRB3 in renal mesangial cells. TRB3 may be involved in diabetic nephropathy by regulating the fibrosis cytokine TGF-β1 and collagen type IV through the ERK1/2 MAPK signaling pathway.