Rosuvastatin inhibits high glucose-stimulated upregulation of VCAM-1 via the MAPK-signalling pathway in endothelial cells. Issue 1 (2nd January 2018)

• Record Type: Journal Article
• Authors: Kim, Moo Hyun; Kim, Chae-Eun; Kim, Sung-Whan
• Is Part Of: Acta cardiologica. Volume 73:Issue 1(2018)
• Page Start: 13
• Page End: 18
• Publication Date: 2018-01-02
• Subjects: Adhesion -- endothelial cells -- MAPK pathway -- rosuvastatin; Cardiology -- Periodicals; Cardiology; Cardiologie -- Périodiques; Cardiology; Cardiologie; Periodicals; Periodicals; 616.12005
• DOI: 10.1080/00015385.2017.1321908
• Languages: English
• ISSNs: 0001-5385

Abstract

Abstract: Objective: The aim of this study is to investigate the molecular mechanisms and effect of rosuvastatin on adhesion molecule induction in human endothelial cells under high-glucose conditions (HG). Methods and results: The effects of rosuvastatin on vascular cell adhesion molecule (VCAM)-1 production and pERK phosphorylation were measured in HG-induced human umbilical vein endothelial cells (HUVECs) with inhibitors targeting the mitogen-activated protein kinase (MAPK) signal pathway. HG increased levels of VCAM-1. Treatment with rosuvastatin inhibited VCAM-1 expression in a concentration- and time-dependent manner. In addition, we investigated the effects of rosuvastatin on the extracellular signal-regulated kinase (ERK) 1/2 signal pathway. Rosuvastatin completely inhibited HG-induced phosphorylation of ERK. ERK/MAPK inhibitors completely prevented the VCAM-1 inhibition effect of rosuvastatin under HG condition. Conclusions: This study demonstrated that rosuvastatin suppresses HG-induced VCAM-1 production via the MAPK signalling pathway, playing a role in the suppression of atherosclerosis.