Advanced oxidation protein products induce monocyte chemoattractant protein-1 expression via p38 mitogen-activated protein kinase activation in rat vascular smooth muscle cells.

Full Abstract

BACKGROUND:
Advanced oxidation protein products (AOPPs) are new uremic toxins reported by Witko-Sarsat in 1996, which are associated with the pathogenesis of atherosclerosis. However, the mechanisms by which AOPPs enhance atherosclerosis have not been fully understood. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine which stimulates migration of monocytes and plays a critical role in the development of atherosclerosis. In this study, we investigated the effect of AOPPs on MCP-1 expression in cultured vascular smooth muscle cells (VSMCs).

METHODS:
VSMCs were cultured and then co-incubated with AOPP (200 micromol/L, 400 micromol/L) for different times with or without pretreatment with specific p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. RT-PCR and Western blott were used to detect MCP-1 mRNA and protein expression at different time points after AOPP stimulation in rat smooth muscle cells. Western blot was used to detect the expression of phosphorylated p38 MAPK.

RESULTS:
Treatment of VSMC with AOPPs resulted in a significant increase of the expression of MCP-1 mRNA and protein in time- and dose-dependent manner, and could activated p38 MAPK. Pretreatment of VSMCs with SB203580 resulted in a dose-dependent inhibition of AOPPs-induced MCP-1 mRNA and protein expression.

CONCLUSIONS:
AOPPs can stimulate MCP-1 expression via p38 MAPK in VSMCs. This suggests that AOPPs might contribute to the formation of atherosclerosis through this proinflammatory effect.

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Author information

Author/s: Peng, Kan-fu (KF); Wu, Xiong-fei (XF); Zhao, Hong-wen (HW); Sun, Yan (Y);

Affiliation: Department of Nephrology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

Journal and publication information

Publication Type: Journal Article

Journal: Chinese medical journal (Chin Med J (Engl)), published in China. (Language: eng)

Reference: 2006-Jul; vol 119 (issue 13) : pp 1088-93

Dates: Created 2006/07/12; Completed 2006/08/09; Revised 2006/11/15;

PMID: 16834927, status: MEDLINE (last retrieval date: 12/26/2008)

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals
Atherosclerosis - etiology
Cardiovascular Diseases - etiology
Cells, Cultured
Chemokine CCL2 - genetics
Enzyme Activation
Imidazoles - pharmacology
Kidney Failure, Chronic - complications
Male
Muscle, Smooth, Vascular - cytology; metabolism

Muscle, Smooth, Vascular - cytology; metabolism
Myocytes, Smooth Muscle - metabolism
Oxidation-Reduction
Proteins - metabolism
Pyridines - pharmacology
RNA, Messenger - analysis
Rats
Rats, Sprague-Dawley
Uremia - metabolism
p38 Mitogen-Activated Protein Kinases - physiology

Associated Chemicals: Chemokine CCL2 (0) ; Imidazoles (0) ; Proteins (0) ; Pyridines (0) ; RNA, Messenger (0) ; SB 203580 (0) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.1.37)

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