Document Detail


Increased protein O-GlcNAc modification inhibits inflammatory and neointimal responses to acute endoluminal arterial injury.
MedLine Citation:
PMID:  18469144     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Inflammation plays a major role in vascular disease. We have shown that leukocyte infiltration and inflammatory mediator expression contribute to vascular remodeling after endoluminal injury. This study tested whether increasing protein O-linked-N-acetylglucosamine (O-GlcNAc) levels with glucosamine (GlcN) and O-(2-acetamido-2-deoxy-d-glucopyranosylidene) amino-N-phenylcarbamate (PUGNAc) inhibits acute inflammatory and neointimal responses to endoluminal arterial injury. Ovariectomized rats were treated with a single injection of GlcN (0.3 mg/g ip), PUGNAc (7 nmol/g ip) or vehicle (V) 2 h before balloon injury of the right carotid artery. O-GlcNAc-modified protein levels decreased markedly in injured arteries of V-treated rats at 30 min, 2 h, and 24 h after injury but returned to control (contralateral uninjured) levels after 14 days. Both GlcN and PUGNAc increased O-GlcNAc-modified protein levels in injured arteries compared with V controls at 30 min postinjury; the GlcN-mediated increase persisted at 24 h but was not evident at 14 days. Proinflammatory mediator expression increased markedly after injury and was reduced significantly (30-50%) by GlcN and PUGNAc. GlcN and PUGNAc also inhibited infiltration of neutrophils and monocytes in injured arteries. Chronic (14 days) treatment with GlcN reduced neointima formation in injured arteries by 50% compared with V controls. Acute GlcN and PUGNAc treatment increases O-GlcNAc-modified protein levels and inhibits acute inflammatory responses in balloon-injured rat carotid arteries; 14 day GlcN treatment inhibits neointima formation in these vessels. Augmenting O-GlcNAc modification of proteins in the vasculature may represent a novel anti-inflammatory and vasoprotective mechanism.
Authors:
Dongqi Xing; Wenguang Feng; Laszlo G Nöt; Andrew P Miller; Yun Zhang; Yiu-Fai Chen; Erum Majid-Hassan; John C Chatham; Suzanne Oparil
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-05-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  295     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-07-15     Completed Date:  2008-08-21     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H335-42     Citation Subset:  IM    
Affiliation:
Department of Medicine, Univ. of Alabama at Birmingham, Birmingham, Alabama 35294, USA. dqxing@uab.edu
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MeSH Terms
Descriptor/Qualifier:
Acetylglucosamine / analogs & derivatives*,  pharmacology
Animals
Anti-Inflammatory Agents / pharmacology*
Carotid Arteries / drug effects*,  metabolism,  pathology
Carotid Artery Injuries / drug therapy*,  metabolism,  pathology
Disease Models, Animal
Female
Glucosamine / pharmacology*
Glycosylation
Inflammation Mediators / metabolism*
Monocytes / drug effects,  metabolism
Neutrophil Infiltration / drug effects
Ovariectomy
Oximes / pharmacology*
Phenylcarbamates / pharmacology*
Protein Processing, Post-Translational / drug effects*
Rats
Rats, Sprague-Dawley
Time Factors
Grant Support
ID/Acronym/Agency:
HL-044195/HL/NHLBI NIH HHS; HL-067464/HL/NHLBI NIH HHS; HL-07457/HL/NHLBI NIH HHS; HL-076175/HL/NHLBI NIH HHS; HL-079364/HL/NHLBI NIH HHS; HL-080017/HL/NHLBI NIH HHS; HL-64614/HL/NHLBI NIH HHS; HL-68806/HL/NHLBI NIH HHS; HL-75211/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Inflammation Mediators; 0/Oximes; 0/Phenylcarbamates; 132489-69-1/N-acetylglucosaminono-1,5-lactone O-(phenylcarbamoyl)oxime; 3416-24-8/Glucosamine; 7512-17-6/Acetylglucosamine
Comments/Corrections

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


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