Mechanism of eNOS gene transfer inhibition of vascular smooth muscle cell proliferation.

Authors: D'Souza, FM  Sparks, RL  Chen, H  Kadowitz, PJ  Jeter JR, JR 
Citation: D'Souza FM, etal., Am J Physiol Cell Physiol 2003 Jan;284(1):C191-9.
Pubmed: (View Article at PubMed) PMID:12388111
DOI: Full-text: DOI:10.1152/ajpcell.00179.2002

Endothelial nitric oxide synthase (eNOS) is responsible for the production of nitric oxide (NO) in blood vessels. NO has been shown to be involved in the inhibition of vascular smooth muscle cell (VSMC) proliferation. In the present study, the eNOS gene was transferred into rat aortic smooth muscle cells by using an adenoviral vector, and the effect of endogenously produced NO on VSMC proliferation was investigated. The presence of eNOS in eNOS-transfected cells was confirmed by immunocytochemistry and Western blot analysis. eNOS transfection resulted in inhibition of VSMC proliferation. This effect was accompanied by increased levels of p53 and p21. This effect was abrogated in the presence of the protein kinase A (PKA) inhibitor Rp-8-bromoadenosine 3',5'-cyclic monophosphothioate. The increased levels of p53 and p21 observed in eNOS-transfected cells were reduced in the presence of the PKA inhibitor. These data suggest that p21 and p53 play a role in the inhibition of proliferation in eNOS-transfected cells and that levels of these two proteins are regulated by PKA.


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CRRD Object Information
CRRD ID: 628542
Created: 2003-02-05
Species: All species
Last Modified: 2003-02-05
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.