Golgi apparatus fragmentation participates in oxidized low-density lipoprotein-induced endothelial cell injury.

Abstract:

:Oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury plays crucial roles in the development of arteriosclerosis (AS). Golgi apparatus (GA) fragmentation is involved in various pathological processes, including endothelial injury. However, the role of GA fragmentation in ox-LDL-induced endothelial injury has not been determined. In this study, human umbilical vein endothelial cells (HUVECs) subjected to ox-LDL were used as an in vitro AS model. Herein, we showed that ox-LDL restrained proliferation and induced apoptosis and GA fragmentation of HUVECs. Moreover, overexpression of GRASP65 significantly prevented ox-LDL-induced GA fragmentation and endothelial cell injury by enhancing cell viability, nitric oxide production, and endothelial NOS expression and reducing apoptosis. Mechanistically, ox-LDL resulted in the activation of the extracellular signal-regulated kinase (ERK) pathway in HUVECs. Inactivation of the ERK pathway by U0126 suppressed the phosphorylation of GRASP65, GA fragmentation, and endothelial cell injury induced by ox-LDL. In conclusion, ox-LDL triggers GA fragmentation in HUVECs via activating the ERK signaling pathway, which participates in endothelial injury during the development of AS.

journal_name

J Cell Biochem

authors

Ji G,Song X,Wang L,Li Z,Wu H,Dong H

doi

10.1002/jcb.29205

subject

Has Abstract

pub_date

2019-11-01 00:00:00

pages

18862-18870

issue

11

eissn

0730-2312

issn

1097-4644

journal_volume

120

pub_type

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