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Suppressor of cytokine signaling‐1 reduces high glucose‐induced TGF‐β1 and fibronectin synthesis in human mesangial cells
Author(s) -
Shi Yonghong,
Zhang Yanling,
Wang Chen,
Du Chunyang,
Zhao Song,
Qi Zhao,
Zhang Qingxian,
Duan Huijun
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.09.014
Subject(s) - fibronectin , cytokine , transforming growth factor , suppressor , chemistry , signal transduction , suppressor of cytokine signaling 1 , microbiology and biotechnology , cancer research , endocrinology , immunology , biology , biochemistry , gene , cell
Janus kinase (JAK) signal transducers, and activators of transcription (STAT), contribute to diabetic nephropathy. Here we show that one of the suppressors of cytokine signaling (SOCS) proteins, SOCS‐1, was upregulated in human mesangial cells (HMCs) under high glucose conditions, along with the activation of JAK2, STAT1, and STAT3. Overexpression of SOCS‐1 in HMCs inhibited HG‐induced JAK2/STAT activation, c‐Fos/c‐Jun expression, and increased synthesis of TGF‐β1 and fibronectin. These data suggest that SOCS‐1 inhibits HG‐induced overexpression of TGF‐β1 and synthesis of fibronectin in HMC, which may be via JAK/STAT pathway.