Document Detail


Increased methylglyoxal and oxidative stress in hypertensive rat vascular smooth muscle cells.
MedLine Citation:
PMID:  11897769     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Methylglyoxal can yield advanced glycation end products via nonenzymatic glycation of proteins. Whether methylglyoxal contributes to the pathogenesis of hypertension has not been clear. The aim of the present study was to investigate whether the levels of methylglyoxal and methylglyoxal-induced advanced glycation end products were enhanced and whether methylglyoxal increased oxidative stress, activated nuclear factor-kappaB (NF-kappaB), and increased intracellular adhesion molecule-1 (ICAM-1) content in vascular smooth muscle cells from spontaneously hypertensive rats. Basal cellular levels of methylglyoxal and advanced glycation end products were more than 2-fold higher (P<0.05) in cells from hypertensive rats than from normotensive Wistar-Kyoto rats. This correlated with levels of oxidative stress and oxidized glutathione that were significantly higher in cells from hypertensive rats, whereas levels of glutathione and activities of glutathione reductase and glutathione peroxidase were significantly lower. Basal levels of nuclearly localized NF-kappaB p65 and ICAM-1 protein expression were higher in cells from hypertensive rats than from normotensive rats. Addition of exogenous methylglyoxal to the cultures induced a greater increase in oxidative stress and advanced glycation end products in cells from hypertensive rats compared with normotensive rats and significantly decreased the activities of glutathione reductase and glutathione peroxidase in cells of both rat strains. Methylglyoxal activated NF-kappaB p65 and increased ICAM-1 expression in hypertensive cells, which was inhibited by N-acetylcysteine. Our study demonstrates an elevated methylglyoxal level and advanced glycation end products in cells from hypertensive rats, and methylglyoxal increases oxidative stress, activates NF-kappaB, and enhances ICAM-1 expression. Our findings suggest that that elevated methylglyoxal and associated oxidative stress possibly contribute to the pathogenesis of hypertension.
Authors:
Lingyun Wu; Bernhard H J Juurlink
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hypertension     Volume:  39     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-03-18     Completed Date:  2002-05-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  809-14     Citation Subset:  IM    
Affiliation:
Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cells, Cultured
Fluoresceins / metabolism
Glutathione / metabolism
Glutathione Peroxidase / metabolism
Glutathione Reductase / metabolism
Glutathione Transferase / metabolism
Glycosylation End Products, Advanced / metabolism*
Hypertension / metabolism*
Intercellular Adhesion Molecule-1 / metabolism
Muscle, Smooth, Vascular / cytology,  metabolism*
NF-kappa B / metabolism
Oxidation-Reduction
Oxidative Stress
Pyruvaldehyde / metabolism*
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Species Specificity
Chemical
Reg. No./Substance:
0/Fluoresceins; 0/Glycosylation End Products, Advanced; 0/NF-kappa B; 106070-31-9/2',7'-dichlorodihydrofluorescein; 126547-89-5/Intercellular Adhesion Molecule-1; 70-18-8/Glutathione; 78-98-8/Pyruvaldehyde; EC 1.11.1.9/Glutathione Peroxidase; EC 1.8.1.7/Glutathione Reductase; EC 2.5.1.18/Glutathione Transferase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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