RGD Reference Report - Resveratrol inhibits neointimal formation after arterial injury through an endothelial nitric oxide synthase-dependent mechanism. - Rat Genome Database

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Resveratrol inhibits neointimal formation after arterial injury through an endothelial nitric oxide synthase-dependent mechanism.

Authors: Breen, DM  Dolinsky, VW  Zhang, H  Ghanim, H  Guo, J  Mroziewicz, M  Tsiani, EL  Bendeck, MP  Dandona, P  Dyck, JR  Heximer, SP  Giacca, A 
Citation: Breen DM, etal., Atherosclerosis. 2012 Jun;222(2):375-81. Epub 2012 Mar 27.
RGD ID: 6484736
Pubmed: PMID:22552115   (View Abstract at PubMed)
DOI: DOI:10.1016/j.atherosclerosis.2012.03.021   (Journal Full-text)

Revascularization procedures used for treatment of atherosclerosis often result in restenosis. Resveratrol (RSV), an antioxidant with cardiovascular benefits, decreases neointimal formation after arterial injury by a mechanism that is still not fully clarified. Our main objective was to address the role of nitric oxide synthases (NOSes) and more specifically the endothelial-NOS (eNOS) isoform as a mediator of this effect. RSV (4mg/kg/day, s.c.) alone or in combination with the NOS inhibitor N-nitro-l-arginine methyl ester (l-NAME) (2mg/kg/day, s.c.) was given to Sprague-Dawley rats beginning at 3 days before arterial (carotid or aortic) injury. RSV reduced neointimal formation by 50% (P<0.01), decreased intimal cell proliferation by 37% (P<0.01) and reduced inflammatory markers such as PECAM and MMP-9 mRNA. These effects of RSV were all abolished by coadministration of l-NAME. Oral RSV (beginning at 5 days before arterial injury) reduced neointimal thickness after femoral wire injury in mice, however this effect was not observed in eNOS knockout mice. This is the first report of RSV decreasing neointimal cell proliferation and neointimal growth through an eNOS-dependent mechanism.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MMP9HumanArterial Injury treatmentISOMmp9 (Rattus norvegicus) RGD 
Mmp9RatArterial Injury treatmentIDA  RGD 
Mmp9MouseArterial Injury treatmentISOMmp9 (Rattus norvegicus) RGD 
PECAM1HumanVascular System Injuries  ISOPecam1 (Rattus norvegicus) RGD 
Pecam1RatVascular System Injuries  IDA  RGD 
Pecam1MouseVascular System Injuries  ISOPecam1 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mmp9  (matrix metallopeptidase 9)
Pecam1  (platelet and endothelial cell adhesion molecule 1)

Genes (Mus musculus)
Mmp9  (matrix metallopeptidase 9)
Pecam1  (platelet/endothelial cell adhesion molecule 1)

Genes (Homo sapiens)
MMP9  (matrix metallopeptidase 9)
PECAM1  (platelet and endothelial cell adhesion molecule 1)


Additional Information