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首页> 外文期刊>Cytokine >High glucose induces mitochondrial dysfunction and apoptosis in human retinal pigment epithelium cells via promoting SOCS1 and Fas/FasL signaling
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High glucose induces mitochondrial dysfunction and apoptosis in human retinal pigment epithelium cells via promoting SOCS1 and Fas/FasL signaling

机译：高糖通过促进SOCS1和Fas / FasL信号传导诱导人视网膜色素上皮细胞线粒体功能障碍和凋亡

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Diabetic retinopathy (DR) is one of the most serious complications of diabetes mellitus (DM), however, the contribution of high glucose (HG) or hyperglycemia to DR is far from fully understanding. In the present study, we examined the expression of Fas/FasL signaling and suppressors of cytokine signaling (SOCS)1 and 3 in HG-induced human retinal pigment epithelium cells (ARPE-19 cells). And then we investigated the regulatory role of both Fas and SOCS1 in HG-induced mitochondrial dysfunction and apoptosis. Results demonstrated that HG with more than 40 mM induced mitochondrial dysfunction via reducing mitochondrial membrane potential (MMP) and via inhibiting the Bcl-2 level, which is the upstream signaling of mitochondria in ARPE-19 cells. HG also upreuglated the Fas signaling and SOCS levels probably via promoting JAK/STAT signaling in ARPE-19 cells. Moreover, the exogenous Fas or entogenous overexpressed SOCS1 accentuated the HG-induced mitochondrial dysfunction and apoptosis, whereas the knockdown of either Fas or SOCS1 reduced the HG-induced mitochondria dysfunction and apoptosis. Thus, the present study confirmed that both Fas/FasL signaling and SOCS1 promoted the HG-induced mitochondrial dysfunction and apoptosis. These results implies the key regulatory role of Fas signaling and SOCS in DR. (C) 2015 Elsevier Ltd. All rights reserved.
机译：糖尿病性视网膜病（DR）是糖尿病（DM）最严重的并发症之一，但是，高血糖（HG）或高血糖症对DR的贡献远未得到充分理解。在本研究中，我们检查了HG诱导的人视网膜色素上皮细胞（ARPE-19细胞）中Fas / FasL信号的表达和细胞因子信号的抑制因子（SOCS）1和3的表达。然后，我们研究了Fas和SOCS1在HG诱导的线粒体功能障碍和细胞凋亡中的调控作用。结果表明，具有40 mM以上的HG通过降低线粒体膜电位（MMP）和抑制Bcl-2水平来诱导线粒体功能障碍，Bcl-2水平是ARPE-19细胞中线粒体的上游信号。 HG还可能通过促进ARPE-19细胞中的JAK / STAT信号传导来上调Fas信号传导和SOCS水平。此外，外源性Fas或内源性过表达的SOCS1加剧了HG诱导的线粒体功能障碍和细胞凋亡，而敲除Fas或SOCS1降低了HG诱导的线粒体功能障碍和细胞凋亡。因此，本研究证实Fas / FasL信号和SOCS1均可促进HG诱导的线粒体功能障碍和细胞凋亡。这些结果暗示了Fas信号和SOCS在DR中的关键调控作用。 （C）2015 Elsevier Ltd.保留所有权利。

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