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Am J Physiol Cell Physiol (September 18, 2002). doi:10.1152/ajpcell.00179.2002
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Articles in PresS, published online ahead of print September 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00179.2002
Submitted on April 18, 2002
Accepted on August 19, 2002

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

Fiona M D'Souza1, Rodney L Sparks2, Huiying Chen2, Philip J Kadowitz3, and James R Jeter, Jr.2*

1 Structural and Cellular Biology, Tulane University Health Sciences Center, New Orleans, LA, USA; Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA, USA
2 Structural and Cellular Biology, Tulane University Health Sciences Center, New Orleans, LA, USA
3 Pharmacology, Tulane University Health Sciences Center, New Orleans, LA, USA

* To whom correspondence should be addressed. E-mail: jjeter{at}tulane.edu.

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 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 an 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-bromo-cAMPS. 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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