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Am J Physiol Regul Integr Comp Physiol (January 16, 2003). doi:10.1152/ajpregu.00434.2002
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Submitted on July 19, 2002
Accepted on January 13, 2003

Relative contribution of the TNF{alpha} receptors to murine intimal hyperplasia

Michael A Zimmerman1, Leonid L Reznikov2, Amy C Sorensen1, and Craig H Selzman1*

1 Division of Cardiothoracic Surgery, University of Colorado Department of Surgery, Denver, Colorado, USA
2 Division of Infectious Disease, University of Colorado Department of Surgery, Denver, Colorado, USA

* To whom correspondence should be addressed. E-mail: craig.selzman{at}uchsc.edu.

Tumor necrosis factor alpha (TNF{alpha}) is an important mediator in the inflammatory response to vascular injury. The current study sought to determine the relative contribution of each TNF{alpha} receptor subtype (p55 and p75) to intimal hyperplasia (IH) and characterize the mechanisms of transcriptional regulation following vascular injury. A murine model of wire carotid arterial injury was employed to induce IH in wild type (WT), p55-deficient (p55 -/-), and p75-deficient (p75 -/-) mice. Compared to injured WT and p75 -/- animals, p55 -/- mice demonstrated a 2-fold reduction in IH. Additionally, p55 -/- mice demonstrated a decrease in expression of nuclear factor kappa-B (NF{kappa}B) mRNA and protein. These observations suggest an important role for the p55 receptor in IH following mechanical endoluminal injury. Suppression of the transcriptional activator NF{kappa}B may provide a mechanism by which p55-mediated IH is attenuated.




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