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Ox-LDL plays dual effect in modulating expression of inflammatory molecules through LOX-1 pathway in human umbilical vein endothelial cells
Huilian Zhu1,Min Xia1,Mengjun Hou1,Zhihong Tang1,Yan Li1,Jing Ma1,Wenhua Ling1
1
School of Public Health, Sun-yat-sen University, 74th Zhongshan Road 2, Guangdong, Guangzhou, 510080, PR China
DOI: 10.2741/1722 Volume 10 Issue 3, pp.2585-2594
Published: 01 September 2005
Abstract

Lectin-like oxidized low-density lipoprotein receptor1 (LOX-1) has been recognized to be the major endothelial receptor for oxidized low-density lipoprotein (ox-LDL). Ox-LDL has been reported to induce the expression of inflammatory adhesive molecules from vascular endothelium. However, the mechanism of this action has not been fully elucidated. Peroxisome proliferation-activated receptor-gamma (PPARgamma) regulates the expression of inflammatory adhesive molecules. The present study was carried out to investigate the role of LOX-1-PPARgamma pathway in regulating expression of adhesion molecules, ICAM-1 and E-selectin in HUVECs. Ox-LDL increased the expression of ICAM-1 and E-selectin in a concentration (10-50 microg/ml)--and time (6-36 hours)--dependent manners. These effects were significantly inhibited by pretreatment of HUVECs with polyinosonic acid or carrageenan. Preincubating HUVECs with 15d-PGJ2 attenuated the expression of ICAM-1 and E-selectin in response to ox-LDL, although ox-LDL stimulated the expression of PPARgamma. Upregulation of ICAM-1 and E-selectin mediated by ox-LDL were inhibited more significantly by the combination of 15d-PGJ2 and polyinosonic acid as compared to either 15d-PGJ2 or polyinosonic acid alone. The results suggested that ox-LDL through its receptor LOX-1 promotes pro-inflammation response by increasing expression of ICAM-1 and E-selectin, simultaneously activates PPARgamma triggering cellular anti-inflammation response in protection from the inflammation lesions in HUVECs.

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Huilian Zhu, Min Xia, Mengjun Hou, Zhihong Tang, Yan Li, Jing Ma, Wenhua Ling. Ox-LDL plays dual effect in modulating expression of inflammatory molecules through LOX-1 pathway in human umbilical vein endothelial cells. Frontiers in Bioscience-Landmark. 2005. 10(3); 2585-2594.