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ELABELA improves endothelial cell function via the ELA–APJ axis by activating the PI3K/Akt signalling pathway in HUVECs and EA.hy926 cells
Author(s) -
Wang Xiujuan,
Liang Guoqing,
Guo Qing,
Cai Wei,
Zhang Xin,
Ni Jianmei,
Tao Yanyan,
Niu Xiulong,
Chen Shaobo
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13382
Subject(s) - wortmannin , pi3k/akt/mtor pathway , protein kinase b , umbilical vein , receptor , downregulation and upregulation , apelin , microbiology and biotechnology , medicine , chemistry , pharmacology , signal transduction , biology , biochemistry , in vitro , gene
Destruction of endothelial cells (ECs) function is involved in the structural and functional pathophysiological processes of preeclampsia (PE). Vascular endothelial injury may pre‐exist for several years in women that develop PE and may pose increased risks for hypertension, coronary artery disease, and type‐2 diabetes mellitus. Previous findings showed that Elabela (ELA), the endogenous ligand of the apelin (APJ) receptor expressed mainly on ECs, may play a protective role in early pregnancy and prevent PE. However, the exact functional role and molecular mechanisms of ELA are unclear. Here, we aimed to classify whether and how ELA improves EC function via the ELA–APJ axis. Two human umbilical vein endothelial cell (HUVEC) lines, namely HUVECs and EA.hy926, were treated with ELA, and then their cellular activities were studied by performing CCK‐8 tests, scratch‐wound analysis, and tube‐formation assays. Doses of ELA exceeding 0.01 μmol/L markedly improved the cell viability, migration, and tube formation ability of HUVECs and EA.hy926 cells. Western blot analysis indicated that the above effects caused by ELA were related to upregulation of the APJ receptor and activation of PI3K/Akt signalling. Further verification tests were performed using the PI3K inhibitor wortmannin, and the results illustrated that inhibiting PI3K/Akt signalling blocked the positive effects of ELA on EC function and APJ receptor expression. Taken together, our findings indicate that ELA may alter EC function via the ELA–APJ axis and PI3K/Akt signalling and that ELA shows promise for use in endothelial dysfunction therapy for preventing and treating PE.