Therapeutic Effects of Suppressors of Cytokine Signaling in Diabetic Nephropathy
Therapeutic Effects of Suppressors of Cytokine Signaling in Diabetic Nephropathy
复制标题
DOI：
10.1369/0022155413512493
复制
发表时间：
2014-02-01
影响因子：
3.2
通讯作者：
Duan, Huijun
中科院分区：
文献类型：
--
作者：
Liu, Qingjuan;Xing, Lingling;Duan, Huijun
炎症是糖尿病肾病（DN）的重要病理生理机制。肾小管上皮细胞-肌成纤维细胞转分化（TEMT）是DN发生的重要事件，可由多种细胞因子诱导。抑瘤素M（Oncostatin M，OSM）是一种炎性细胞因子，可在体外诱导TEMT。细胞因子信号转导抑制因子（SOCS）蛋白是细胞因子信号转导的负反馈调节因子。本研究旨在探讨SOCS在DN中的作用。结果表明，SOCS过表达改善蛋白尿，-SMA和OSM在肾小管上皮细胞的表达，和间质细胞外基质的积累在CD-1小鼠的肾组织。另外，我们前期的研究表明OSM通过激活JAK/STAT信号通路诱导TEMT，而SOCS可抑制该信号通路。这些结果表明，SOCS的过表达在DN中具有治疗作用。
Inflammation is an important pathophysiological mechanism in diabetic nephropathy (DN). Tubular epithelial cell-myofibroblast transdifferentiation (TEMT), which can be induced by many cytokines, is an important event in DN. Oncostatin M (OSM), an inflammatory cytokine, can induce TEMT in vitro. The suppressors of cytokine signaling (SOCS) proteins are negative-feedback regulators of cytokine signaling. The purpose of this study was to investigate the role of SOCS in DN. The results demonstrated that overexpression of SOCS ameliorated proteinuria, the expression of -SMA and OSM in tubular epithelial cells, and interstitial extracellular matrix accumulation in the renal tissue of CD-1 mice. In addition, our previous studies indicated that OSM induced TEMT by activating the JAK/STAT pathway, which could be inhibited by SOCS. These results indicate that overexpression of SOCS has a therapeutic effect in DN.