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Relative contribution of the TNF-alpha receptors to murine intimal hyperplasia. Am J Physiol Regul Integr Comp Physiol 2003 May;284(5):R1213-8

Date

01/18/2003

Pubmed ID

12531783

DOI

10.1152/ajpregu.00434.2002

Scopus ID

2-s2.0-0345269136   17 Citations

Abstract

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-kappaB 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-kappaB may provide a mechanism by which p55-mediated IH is attenuated.

Author List

Zimmerman MA, Reznikov LL, Sorensen AC, Selzman CH

Author

Michael A. Zimmerman MD, FACS Professor in the Surgery department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Antigens, CD
Carotid Artery Injuries
Gene Expression Regulation
Hyperplasia
Male
Mice
Mice, Knockout
NF-kappa B
Receptors, Tumor Necrosis Factor
Receptors, Tumor Necrosis Factor, Type I
Receptors, Tumor Necrosis Factor, Type II
Tumor Necrosis Factor-alpha
Tunica Intima
jenkins-FCD Prod-486 e3098984f26de787f5ecab75090d0a28e7f4f7c0