标题:High-glucose induces cardiac myocytes apoptosis through Foxo1/GRK2 signaling pathway
作者:Yang, Ming; Lin, Yanliang; Wang, Yuan; Wang, Yulin
作者机构:[Yang, Ming] Shandong Univ, Dept Ultrasound, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.; [Lin, Yanliang] Shandong Univ, Shandong P 更多
通讯作者:Wang, Y;Wang, YL
通讯作者地址:[Wang, Y]Shandong Univ, Shandong Prov Hosp, Dept Neurol, Jinan 250021, Shandong, Peoples R China;[Wang, YL]Shandong Univ, Shandong Prov Hosp, Dept Ped 更多
来源:BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
出版年:2019
卷:513
期:1
页码:154-158
DOI:10.1016/j.bbrc.2019.03.193
关键词:Cardiac myocytes; Foxo1; GRK2; Autophagy; ROS; Apoptosis
摘要:High glucose-induced cardiac myocytes apoptosis has been well demonstrated, but the mechanism remains unknown. In this study, we found that exposure of cardiac H9c2 cells to high glucose promoted Foxo1 and GRK2 expression, and induced autophagy. Further investigation showed that high glucose simultaneously increased the expression of cytoplasmic and nuclear Foxol. Inhibition of Foxo1 reduced GRK2 expression and blocked autophagy, enhancing high glucose-induced apoptosis. GRK2 knockdown did not significantly affect Foxo1 expression and autophagy, but attenuated high glucose-induced apoptosis. Intriguingly, GRK2 knockdown reduced ROS generation. NAC treatment not only reduced the levels of cytoplasmic and nuclear Foxo1, but also inhibited GRK2 expression and autophagy, remarkably reducing high glucose-induced apoptosis. Inhibition of autophagy did not notably affect the expression of Foxo1 and GRK2, but enlarged high glucose-induced apoptosis. ChIP assay and Luciferase reporter assay confirmed that Foxo1 positively regulated GRK2 transcription. These results suggested that Foxo1 was involved in glucose-induced apoptosis by regulating GRK2 expression and autophagy. (C) 2019 Elsevier Inc. All rights reserved.
收录类别:SCOPUS;SCIE
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064498880&doi=10.1016%2fj.bbrc.2019.03.193&partnerID=40&md5=d5d9819dd364684cc00e8f60f11173a3
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