| IFN-γ suppresses the high glucose-induced increase in TGF-β1 and CTGF synthesis in mesangial cells. | |
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MedLine Citation:
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PMID: 22180355 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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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. |
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Authors:
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Juan Du; Lining Wang; Linlin Liu; Qiuling Fan; Li Yao; Yan Cui; Ping Kang; Hong Zhao; Xin Feng; Hui Gao |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Pharmacological reports : PR Volume: 63 ISSN: 1734-1140 ISO Abbreviation: Pharmacol Rep Publication Date: 2011 Sep |
Date Detail:
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Created Date: 2011-12-19 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101234999 Medline TA: Pharmacol Rep Country: Poland |
Other Details:
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Languages: eng Pagination: 1137-44 Citation Subset: IM |
Affiliation:
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Department of Nephrology, First Hospital of China Medical University, 155 North Nanjing Street, Shenyang City, Liaoning Province 110001, People's Republic of China. docwln@live.cn. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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