Objective. It has been increasingly appreciated that G protein-coupled estrogen receptor 1 (GPER1) mediates both proinflammatory and anti-inflammatory response of estrogen. It is also involved in some rapid vascular effects of aldosterone in a mineralocorticoid receptor (MR) independent manner. However, whether GPER1 mediates aldosterone-induced inflammation response in endothelial cells and its relationship with MR are yet undetermined and therefore require further explanation. Method. Based on the hypothesis that GPER1 plays a role in the aldosterone-related vascular inflammation, the present study utilized a model of human umbilical vein endothelial cells transfected with MR siRNA and induced for inflammatory response with increasing concentration of aldosterone. Results. It was discovered that induction of aldosterone had no effect on the expression of GPER1 but promoted the expression of MR. Suppression of MR did not influence GPER1 expression, and GPER1 was capable of mediating part of aldosterone-induced endothelial inflammatory response. This effect may involve phosphoinositide 3-kinases (PI3K) pathway signaling. Conclusion. These findings not only demonstrated the role of GPER1 in aldosterone-induced vascular inflammation but also suggested an alternative for pharmaceutical treatment of hyperaldosteronism considering the unsatisfying effect on cardiovascular risks with MR antagonists.

中文翻译：

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G 蛋白偶联雌激素受体 1 (GPER1) 以不依赖盐皮质激素受体的方式介导醛固酮诱导的内皮炎症

客观。人们越来越认识到 G 蛋白偶联雌激素受体 1 (GPER1) 介导雌激素的促炎和抗炎反应。它还以不依赖盐皮质激素受体 (MR) 的方式参与醛固酮的一些快速血管效应。然而，GPER1 是否介导醛固酮诱导的内皮细胞炎症反应及其与 MR 的关系尚未确定，因此需要进一步解释。方法。基于 GPER1 在醛固酮相关血管炎症中起作用的假设，本研究利用人脐静脉内皮细胞模型转染了 MR siRNA，并随着醛固酮浓度的增加而诱导炎症反应。结果. 发现醛固酮的诱导对GPER1的表达没有影响，但促进了MR的表达。抑制 MR 不影响 GPER1 的表达，并且 GPER1 能够介导醛固酮诱导的部分内皮炎症反应。这种效应可能涉及磷酸肌醇 3-激酶 (PI3K) 通路信号传导。结论。这些发现不仅证明了 GPER1 在醛固酮诱导的血管炎症中的作用，而且考虑到 MR 拮抗剂对心血管风险的影响不令人满意，还提出了一种药物治疗醛固酮增多症的替代方法。