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首页> 外文期刊>Journal of biochemical and molecular toxicology >Inhibiting endoplasmic reticulum stress by activation of G-protein-coupled estrogen receptor to protect retinal astrocytes under hyperoxia
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Inhibiting endoplasmic reticulum stress by activation of G-protein-coupled estrogen receptor to protect retinal astrocytes under hyperoxia

机译：通过激活G蛋白偶联雌激素受体来抑制内质网胁迫，以保护高氧化视网膜星形胶质细胞

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摘要

Retinal vascularization is arrested at the early (hyperoxia) stage in retinopathy of prematurity (ROP), a leading cause of blindness in children. Estrogen was reported to alleviate ROP by inhibiting reactive oxygen species, the upstream signaling molecules of endoplasmic reticulum stress (ERS). Astrocytes have long been proposed to guide angiogenesis, because they form a reticular network that provides a substrate for migrating endothelial cells. However, the factors that control the vascularization of the immature retina and the therapeutic mechanism of estrogen in early ROP remain poorly understood. This study aimed to investigate the role of G-protein-coupled estrogen receptor (GPER), an estrogen receptor distributed in the endoplasmic reticulum (ER), in protecting retinal astrocytes under hyperoxia and the association with ERS. The results showed that GPER was widely expressed in retinal astrocytes. GPER activation increases cell viability, decreases apoptosis, and au-tophagy of retinal astrocytes, decreases inositol-l,4,5-triphosphate receptor activity, and increases Ca~2+ concentration in ER of astrocytes under hyperoxia. GPER blockade reversed all of these changes. Together, our findings indicate that GPER can protect the survival of retinal astrocytes by inhibiting ERS under hyperoxia.
机译：早产儿视网膜病变（ROP）是导致儿童失明的主要原因，视网膜血管化在早期（高氧）阶段被阻止。据报道，雌激素通过抑制内质网应激（ERS）的上游信号分子活性氧来缓解ROP。星形胶质细胞长期以来被认为是引导血管生成的物质，因为它们形成网状网络，为内皮细胞的迁移提供基质。然而，控制未成熟视网膜血管化的因素以及早期ROP中雌激素的治疗机制仍不清楚。本研究旨在探讨分布在内质网（ER）中的雌激素受体G蛋白偶联雌激素受体（GPER）在高氧条件下保护视网膜星形胶质细胞中的作用及其与ER的关系。结果表明，GPER在视网膜星形胶质细胞中广泛表达。在高氧条件下，GPER激活可增加细胞活力，减少凋亡和视网膜星形胶质细胞的吞噬，降低肌醇-l，4,5-三磷酸受体活性，并增加星形胶质细胞ER中的Ca~2+浓度。GPER封锁逆转了所有这些变化。总之，我们的研究结果表明，GPER可以通过抑制高氧条件下的ERS来保护视网膜星形胶质细胞的存活。

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