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Inhibition of endoplasmic reticulum stress mediates the ameliorative effect of apelin on vascular calcification

内质网 沃特曼宁 阿佩林 内分泌学 蛋白激酶B 内科学 化学 磷酸化 医学 生物化学 受体
作者
Yanqing Li,Yuqing Li,Ying Li,Ziyuan Yang,Haigang Geng,Chenxi Liu,Wei Hao,Rui Yang,Sheng Jin,Yuming Wu,Xiao‐Ning Wang,Xu Teng
出处
期刊:Journal of Molecular and Cellular Cardiology [Elsevier]
卷期号:152: 17-28 被引量:9
标识
DOI:10.1016/j.yjmcc.2020.11.017
摘要

Aims Apelin is the endogenous ligand of G protein-coupled receptor APJ and play an important role in the regulation of cardiovascular homeostasis. We aimed to investigate whether apelin ameliorates vascular calcification (VC) by inhibition of endoplasmic reticulum stress (ERS). Methods and results VC model in rats was induced by nicotine plus vitamin D, while calcification of vascular smooth muscle cell (VSMC) was induced by beta-glycerophosphate. Alizarin Red S staining showed dramatic calcium deposition in the aorta of rats with VC, while calcium contents and ALP activity also increased in calcified aorta. Protein levels of apelin and APJ were decreased in the calcified aorta. In rats with VC, apelin treatment significantly ameliorated aortic calcification, compliance and stimulation of ERS. The ameliorative effect of apelin on VC and ERS was also observed in calcified VSMCs. ERS stimulator (tunicamycin or DTT) blocked the beneficial effect of apelin. Apelin treatment activated the PI3K/Akt signaling, blockage of which by wortmannin or inhibitor IV prevented the ameliorative effect of apelin, while ERS inhibitor 4-PBA rescued the blockade effect of wortmannin. Akt-induced GSK inhibition prevented the phosphorylation of PERK and IRE1, and the activation of these two major ERS branches. F13A blocked the ameliorative effect of apelin on VC and ERS, which was reversed by treatment with 4-PBA or Akt activator SC79 Conclusions Apelin ameliorated VC by binding to APJ and then prevented ERS activation by stimulating Akt signaling. These results might provide new target for therapy and prevention of VC.
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