CTRP3 inhibits high glucose-induced human glomerular mesangial cell dysfunction
CTRP3 inhibits high glucose-induced human glomerular mesangial cell dysfunction
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DOI：
10.1002/jcb.27859
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发表时间：
2019-04-01
影响因子：
4
通讯作者：
Pan, Yan-zi
中科院分区：
文献类型：
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作者：
Hu, Tian-ying;Li, La-mei;Pan, Yan-zi
C1 q/肿瘤坏死因子相关蛋白-3（CTRP 3）是CTRP家族的成员，并且其血液水平在肥胖和糖尿病的人类和啮齿动物模型中降低。然而，CTRP 3在糖尿病肾病中的作用仍不清楚。本研究旨在观察CTRP 3对高糖诱导的人肾小球系膜细胞（MCs）增殖和细胞外基质（ECM）积累的影响，并探讨其可能的分子机制。我们的结果表明，CTRP 3的表达显着降低HG刺激MC。此外，CTRP 3过表达抑制MC增殖，活性氧水平，和ECM的生产在汞刺激的MC。CTRP 3过表达抑制HG刺激的MC中Janus激酶2/信号转导和转录激活因子3（JAK 2/STAT 3）通路的激活。总之，这些发现表明CTRP 3通过JAK 2/STAT 3信号通路的失活来减弱HG诱导的MC增殖和ECM产生。因此，CTRP 3可能是治疗糖尿病肾病的潜在治疗靶点。
C1q/tumour necrosis factor-related protein-3 (CTRP3) is a member of CTRP family, and its blood level is reduced in human and rodent models of obesity and diabetes. However, the role of CTRP3 in diabetic nephropathy remains unclear. This study was designed to examine the effects of CTRP3 on cell proliferation and extracellular matrix (ECM) accumulation in human glomerular mesangial cells (MCs) in response to high glucose (HG), and explore the potential molecular mechanisms. Our results demonstrated that the expression of CTRP3 was significantly decreased by HG stimulation in MCs. In addition, CTRP3 overexpression inhibited MCs proliferation, reactive oxygen species level, and ECM production in HG-stimulated MCs. Mechanistically, CTRP3 overexpression inhibited the activation of the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) pathway in HG-stimulated MCs. Taken together, these findings indicated that CTRP3 attenuated HG-induced MC proliferation and ECM production through the inactivation of the JAK2/STAT3 signaling pathway. Thus, CTRP3 may be a potential therapeutic target for the treatment of diabetic nephropathy.