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Am J Physiol Regul Integr Comp Physiol 284: R1213-R1218, 2003. First published January 16, 2003; doi:10.1152/ajpregu.00434.2002
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Vol. 284, Issue 5, R1213-R1218, May 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

Divisions of 1 Cardiothoracic Surgery and 2 Infectious Disease, University of Colorado Health Sciences Center, Denver, Colorado 80262

Tumor necrosis factor-alpha (TNF-alpha ) is an important mediator in the inflammatory response to vascular injury. The present 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 after 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 with injured WT and p75-/- animals, p55-/- mice demonstrated a twofold reduction in IH. Additionally, p55-/- mice demonstrated a decrease in expression of nuclear factor-kappa B mRNA and protein. These observations suggest an important role for the p55 receptor in IH after mechanical endoluminal injury. Suppression of the transcriptional activator nuclear factor-kappa B may provide a mechanism by which p55-mediated IH is attenuated.

vasculature; restenosis; carotid arteries


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