Faculty Collaboration Database

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 (requires institutional sign-in at Scopus site)   18 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

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