SENP1-Mediated Desumoylation of DBC1 Inhibits Apoptosis Induced by High Glucose in Bovine Retinal Pericytes.
SENP1-Mediated Desumoylation of DBC1 Inhibits Apoptosis Induced by High Glucose in Bovine Retinal Pericytes.
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DOI：
10.1155/2016/6392658
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发表时间：
2016
影响因子：
1.9
通讯作者：
Xu X
中科院分区：
文献类型：
--
作者：
Gao J;Chen X;Gu Q;Liu X;Xu X
周细胞丢失是糖尿病视网膜病变的早期特征性变化，但其确切的分子机制尚未阐明。本研究探讨了SENP 1在糖尿病视网膜病变周细胞丢失中的作用。我们证明了高浓度的葡萄糖抑制了Sentrin/SUMO特异性蛋白酶1（SENP 1）的表达，这导致了牛视网膜周细胞（BRPC）中DBC 1类小泛素化的增加。此外，SENP 1过表达减弱充血诱导的BPRCs凋亡，SENP 1敲低加重了这种作用。我们还提供了证据表明，DBC 1 sumoylation/desumoylation参与SENP 1调节的细胞凋亡的BRPCs在高糖条件下。了解SENP 1在高糖诱导的周细胞损失的发病机制中的作用有助于阐明未来药物干预的重要靶点。
Pericyte loss is an early characteristic change in diabetic retinopathy, but its precise molecular mechanisms have not been elucidated. This study investigated the role of SENP1 in pericyte loss in diabetic retinopathy. We demonstrated that a high concentration of glucose inhibited the expression of the Sentrin/SUMO-specific protease 1 (SENP1), which resulted in an increase in DBC1 sumoylation in bovine retinal pericytes (BRPCs). Furthermore, SENP1 overexpression attenuated hyperemia-induced apoptosis of BPRCs, and SENP1 knockdown aggravated this effect. We also provide evidence that DBC1 sumoylation/desumoylation is involved in the SENP1-regulated apoptosis of BRPCs under high glucose conditions. Understanding the role of SENP1 in the pathogenesis of high glucose induced pericyte loss could help elucidate important targets for future pharmacological interventions.