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Am J Physiol Cell Physiol (September 18, 2002). doi:10.1152/ajpcell.00211.2002
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Articles in PresS, published online ahead of print September 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00211.2002
Submitted on May 10, 2002
Accepted on September 9, 2002

Overexpression of p73 causes apoptosis in vascular smooth muscle cells: Implications for vascular proliferative diseases

Benjamin B Davis1, Yao Dong1, and Robert H Weiss1*

1 Internal Medicine, Nephrology, University of California., Davis, Davis, CA, USA

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

Abnormal vascular smooth muscle (VSM) cell proliferation contributes to the development of atherosclerosis and its associated disorders, including angioplasty restenosis. The tumor suppressor protein p53 has been linked to the development of atherosclerotic lesions and its homologue, p73, is proving to have contrasting functions in a variety of tissues. As an outgrowth of our previous finding that p73 is increased in serum-stimulated VSM cells and human atherosclerotic tissue, we examined p73 overexpression in VSM cells to elucidate causality of p73 expression with growth response. Overexpression of p73 results in decreased cell cycle transit and is accompanied by apoptosis. The apoptotic changes in p73 overexpressing VSM cells are independent of p53, and are associated with a decrease in levels of p21waf1/cip1. In conjunction with our previous data that p73 is increased in serum-stimulated VSM cells, this work suggests a role for p73 in vascular proliferative diseases.




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