Home HOME General Physiology and Biophysics 2020 General Physiology and Biophysics Vol.39, No.2, 145–155, 2020

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.39, No.2, 145–155, 2020

Title: Inhibition of HES-1 might play a protective role in endothelial cells under cholesterol stimulation via PI3K/AKT signaling pathway
Author: Yun Shi, Ya Su, Chuanli Liu, Jinglong Tao, Hao Fu, Chengzhi Lu

Abstract: The occurrence of atherosclerotic cardiovascular disease (ASCVD) was closely related to low-density lipoprotein (LDL) cholesterol. HES-1 is critical for maintains of stem cells, quiescent cells or cancer cells, and contributes to drug resistance and metastasis of tumor cells. In this study, we established a cell model of HES-1 inhibition and overexpression in Ea.hy 926 cells, and firstly detected the proliferation rete of Ea.hy 926 cells under cholesterol stimulation using MTT assay, and apoptosis of Ea.hy 926 cells were detected using flow cytometry. Expression of HES-1, apoptosis related proteins and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway were detected using Western blotting analysis. The expression of apoptotis related genes were detected using polymerase chain reaction (PCR) method. The concentration of angiogenesis cytokines was detected using enzyme-linked immunosorbent assay (ELISA) method. We found that proliferation of Ea.hy 926 cells was inhibited after stimulation of cholesterol, inhibition of HES-1 expression would reduce this effect. We also found that expression of apoptosis related molecules was increased and expressions of angiogenesis factors were decreased after cholesterol treatment. Besides, we revealed that these effects were mediated via PI3K/AKT signaling pathway, and HES-1 inhibition could increase the activity of this signaling pathway.

Keywords: HES-1 — Cholesterol — Cardiovascular disease — Endothelial cells — Apoptosis
Published online: 26-Mar-2020
Year: 2020, Volume: 67, Issue: 2 Page From: 145, Page To: 155

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