IMR Press / FBL / Volume 10 / Issue 3 / DOI: 10.2741/1722

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Ox-LDL plays dual effect in modulating expression of inflammatory molecules through LOX-1 pathway in human umbilical vein endothelial cells
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1 School of Public Health, Sun-yat-sen University, 74th Zhongshan Road 2, Guangdong, Guangzhou, 510080, PR China
Front. Biosci. (Landmark Ed) 2005, 10(3), 2585–2594; https://doi.org/10.2741/1722
Published: 1 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.

Keywords
LOX-1
PPARgamma
Endothelial Cells
Oxidized Ldl
Adhesion Molecule
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