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Disruption of TGF-β signaling in smooth muscle cell prevents elastase-induced abdominal aortic aneurysm.

Abstract：

:Transforming growth factor-β (TGF-β) signaling has been significantly implicated in the pathogenesis of aneurysm, prominently the initiation and progression of abdominal aortic aneurysm (AAA). Vascular smooth muscle cell (SMC) is the principal resident cell in aortic wall and is essential for its structure and function. However, the role of TGF-β pathway in SMC for the formation of AAA remains unknown. Therefore, the goal of the present study was to investigate the effect of TGF-β pathway in SMC for AAA pathogenesis, by using a genetical smooth muscle-specific (SM-specific) TGF-β type II receptor (Tgfbr2) disruption animal model. Mice deficient in the expression of Tgfbr2 (MyhCre.Tgfbr2(f/f) and MyhCre.Tgfbr2(WT/f)) and their corresponding wild-type background mice (MyhCre.Tgfbr2(WT/WT)) underwent AAA induction by infrarenal peri-adventitial application of elastase. Fourteen days after elastase treatment, the aortas were analyzed and indicated that disruption of 1 or 2 alleles of Tgfbr2 in SMC provided markedly step-wise protection from AAA formation. And elastin degradation, medial SMC loss, macrophage infiltration, and matrix metalloproteinases (MMP) expression were all significantly reduced in Tgfbr2 deletion mice. Our study demonstrated, for the first time, that the TGF-β signaling pathway in SMC plays a critical role in AAA and disruption can prevent the aneurysm formation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Gao F,Chambon P,Offermanns S,Tellides G,Kong W,Zhang X,Li W

doi

10.1016/j.bbrc.2014.10.053

subject

Has Abstract

pub_date

2014-11-07 00:00:00

pages

137-43

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(14)01851-8

journal_volume

454

pub_type

杂志文章

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