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Am J Physiol Regul Integr Comp Physiol 283: R505-R512, 2002. First published March 29, 2002; doi:10.1152/ajpregu.00033.2002
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Vol. 283, Issue 2, R505-R512, August 2002

Lack of TNF-alpha attenuates intimal hyperplasia after mouse carotid artery injury

Michael A. Zimmerman1, Craig H. Selzman1, Leonid L. Reznikov1, Stephanie A. Miller1, Christopher D. Raeburn1, Julie Emmick2, Xianzhong Meng1, and Alden H. Harken1

1 Department of Surgery, University of Colorado Health Sciences Center, Denver 80262; and 2 Source Precision Medicine, Boulder, Colorado 80301

This study sought to determine the influence of tumor necrosis factor-alpha (TNF-alpha ) on intimal hyperplasia (IH) and characterize the mechanisms of transcriptional regulation after vascular injury. A murine model of wire carotid artery injury was employed to induce IH in wild-type (WT) and TNF-alpha -deficient [TNF(-/-)] animals. Three days after injury, TNF-alpha and nuclear factor-kappa B (NF-kappa B) protein expression was markedly increased in the injured WT carotid artery compared to control. Injury increased TNF-alpha and NF-kappa B mRNA expression 100- and 7.5-fold, respectively. Compared with WT specimens, injury in TNF(-/-) animals decreased both NF-kappa B mRNA and protein nearly 7.5- and 4-fold, respectively. Expression of the NF-kappa B-dependent cytokine monocyte chemotactic protein 1 was markedly diminished in injured TNF(-/-) animals. Finally, TNF(-/-) animals demonstrated a sevenfold reduction in IH compared with WT animals. Cumulatively, these data mechanistically link TNF-alpha and NF-kappa B in vivo and suggest an important influence of TNF-alpha on postinjury IH.

cytokine; inflammation; atherogenesis; transcription; nuclear factor-kappa B


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