IFN-γ suppresses the high glucose-induced increase in TGF-β1 and CTGF synthesis in mesangial cells.
Journal Title: Pharmacological Reports - Year 2011, Vol 63, Issue 5
Abstract
Mesangial cells are the main source of renal interstitial fibrosis in diabetic nephropathy (DN). Interferon-γ (IFN-γ) is a key cytokine that may play a potential therapeutic role in reducing fibrosis. Here, we focus on the effects of IFN-γ on human mesangial cells (HMCs) treated with high glucose. This study shows that IFN-γ phosphorylates STAT1, suppresses HMC proliferation, and downregulates mRNA and protein levels of transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) in HMCs treated with high glucose. The regulation of P-STAT1 could change HMC proliferation and the expression of fibrotic cytokines TGF-β1 and CTGF in HMCs. These data indicate that IFN-γ could activate STAT1 to suppress the increase in TGF-β1 and CTGF synthesis in HMCs induced by high glucose. This paper may lead to new therapeutic treatments of DN.
Authors and Affiliations
Juan Du, Lining Wang, Linlin Liu, Qiuling Fan, Li Yao, Yan Cui, Ping Kang, Hong Zhao, Xin Feng, Hui Gao
Keywords
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