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Trends Cardiovasc Med. 2011 Nov;21(8):229-33. doi: 10.1016/j.tcm.2012.05.016.

AIP1 in graft arteriosclerosis.

Author information

1
Interdepartmental Program in Vascular Biology and Therapeutics and the Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA. wang.min@yale.edu

Abstract

Graft arteriosclerosis (GA), the major cause of late cardiac allograft failure, is characterized by a diffuse, concentric arterial intimal hyperplasia composed of infiltrating host T cells, macrophages, and predominantly graft-derived smooth muscle-like cells that proliferate and elaborate extracellular matrix, resulting in luminal obstruction and allograft ischemia. Interferon-γ (IFN-γ), a proinflammatory cytokine produced by effector T cells, is a critical mediator for smooth muscle-like cell proliferation. We have exploited the power of mouse genetics to examine the function of AIP1, a signaling adaptor molecule involved in vascular inflammation, in two newly established IFN-γ-mediated models of GA. Our data suggest that AIP1 inhibits intimal formation in GA by downregulating IFN-γ-activated migratory and proliferative signaling pathways in smooth muscle-like cells.

PMID:
22902071
PMCID:
PMC3424482
DOI:
10.1016/j.tcm.2012.05.016
[Indexed for MEDLINE]
Free PMC Article

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