Eva1a ameliorates atherosclerosis by promoting re-endothelialization of injured arteries via Rac1/Cdc42/Arpc1b
Eva1a ameliorates atherosclerosis by promoting re-endothelialization of injured arteries via Rac1/Cdc42/Arpc1b
复制标题
Eva1a 通过 Rac1/Cdc42/Arpc1b 促进受损动脉的再内皮化，从而改善动脉粥样硬化
DOI：
10.1093/cvr/cvaa011
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发表时间：
2021-02-01
影响因子：
10.8
通讯作者：
Zheng, Lemin
中科院分区：
文献类型：
--
作者：
Li, Jingxuan;Chen, Yingyu;Zheng, Lemin
Aims Eva-1 homologue 1 (Eva1a) is a novel protein involved in the regulation of cardiac remodelling and plaque stability, but little is known about its role in re-endothelialization and the development of atherosclerosis (AS). Thus, in the present study, we aimed to elucidate the function of Eva1a in re-endothelialization and AS.Methods and results Wire injuries of carotid and femoral arteries were established in Eva1a(-/-) mice. Eva1a-deficient mice were crossed with apolipoprotein E-/- (ApoE(-/-)) mice to evaluate AS development and re-endothelialization of carotid artery injuries. Denudation of the carotid artery at 3, 5, and 7 days was significantly aggravated in Eva1a(-/-) mice. The neointima of the femoral artery at 14 and 28 days was consequently exacerbated in Eva1a(-/-) mice. The area of atherosclerotic lesions was increased in Eva1a(-/-) ApoE(-/-) mice. To explore the underlying mechanisms, we performed transwell, scratch migration, cell counting kit-8, and bromodeoxyuridine assays using cultured human aorta endothelial cells (HAECs), which demonstrated that EVA1A promoted HAEC migration and proliferation. Proteomics revealed that the Level of actin-related protein 2/3 complex subunit 1B (Arpc1b) was decreased, while Evala expression was absent. Arpc1b was found to be a downstream molecule of EVA1A by small interfering RNA transfection assay. Activation of Rac1 and Cdc42 GTPases was also regulated by EVA1A.Conclusion This study provides insights into anti-atherogenesis effects of Eva1a by promoting endothelium repair. Thus, Eva1a is a promising therapeutic target for AS.
