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自发性高血压大鼠视网膜和脉络膜内皮表面分子减少。

Decreased retinal and choroidal endothelial surface molecules in spontaneously hypertensive rats.

机构信息

Louisiana State University Health Sciences Center at Shreveport, Department of Molecular & Cellular Physiology, Shreveport, Louisiana, USA.

Louisiana State University Health Sciences Center at Shreveport, Department of Molecular & Cellular Physiology, Shreveport, Louisiana, USA.

出版信息

Exp Eye Res. 2023 Sep;234:109617. doi: 10.1016/j.exer.2023.109617. Epub 2023 Aug 17.

Abstract

Hypertension is associated with changes in the retina and choroid, with resulting consequences of increased vascular permeability and microhemorrhages. To date, very little information is available regarding the changes in the retinal and choroidal endothelial surface layer. In this study, we have examined changes in protein expression of several molecules including platelet endothelial cell adhesion molecule-1 (PECAM-1), vascular endothelial cadherin (VE-cadherin), glypican-1, and syndecan-1, in spontaneously hypertensive rats (SHR) compared to control normotensive Wistar Kyoto (WKY) rats. In male SHR vs WKY rat retinas, decreases were found for VE-cadherin and syndecan-1; whereas in female retinas, decreases were found for PECAM-1, glypican-1, and syndecan-1. In male SHR vs WKY rat choroid, we found an increase in glypican-1, but choroidal syndecan-1 was decreased in SHR in both males and females. Therefore, decreases in SHR of both retinal and choroidal syndecan-1 were found in both males and females. These losses of syndecan-1 were accompanied by an increase in plasma levels of the proteoglycan, indicating possible systemic endothelial shedding. In contrast, plasma levels of glypican-1 decreased. Interestingly, in normotensive WKY rats, retinal levels of all four endothelial surface molecules were higher in females than in males, in some cases, by substantial amounts. In summary, a number of changes occur in endothelial surface molecules in SHR, with some changes being sex-dependent; it is possible that the loss of these molecules contributes to the vascular dysfunction that occurs in hypertensive retina and choroid.

摘要

高血压与视网膜和脉络膜的变化有关,导致血管通透性增加和微出血等后果。迄今为止,关于视网膜和脉络膜内皮表面层的变化,我们知之甚少。在这项研究中,我们检查了几种分子的蛋白质表达变化,包括血小板内皮细胞黏附分子-1(PECAM-1)、血管内皮钙黏蛋白(VE-cadherin)、聚糖-1 和 syndecan-1,在自发性高血压大鼠(SHR)与对照正常血压 Wistar Kyoto(WKY)大鼠进行比较。与 WKY 大鼠相比,雄性 SHR 视网膜中 VE-cadherin 和 syndecan-1 的表达减少;而在雌性视网膜中,PECAM-1、glypican-1 和 syndecan-1 的表达减少。在雄性 SHR 与 WKY 大鼠脉络膜中,我们发现 glypican-1 增加,但在雄性和雌性 SHR 脉络膜中,syndecan-1 减少。因此,无论是雄性还是雌性 SHR,视网膜和脉络膜的 syndecan-1 都减少了。这些 syndecan-1 的丢失伴随着蛋白聚糖的血浆水平增加,表明可能存在系统性内皮脱落。相反,glypican-1 的血浆水平下降。有趣的是,在正常血压的 WKY 大鼠中,雌性视网膜中所有四种内皮表面分子的水平都高于雄性,在某些情况下,差异很大。总之,SHR 内皮表面分子发生了许多变化,有些变化是性别依赖性的;这些分子的丢失可能导致高血压视网膜和脉络膜中发生的血管功能障碍。

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本文引用的文献

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