Genetic Deletion of Socs3 in Smooth Muscle Cells Ameliorates Aortic Dissection in Mice

被引：18

作者：

Hirakata, Saki ^{[1
]}

Aoki, Hiroki ^{[2
]}

Ohno-Urabe, Satoko ^{[1
]}

Nishihara, Michihide ^{[1
]}

Furusho, Aya ^{[1
]}

Nishida, Norifumi ^{[1
]}

Ito, Sohei ^{[1
]}

Hayashi, Makiko ^{[1
]}

Yasukawa, Hideo ^{[1
]}

Imaizumi, Tsutomu ^{[3
]}

Hiromatsu, Sinichi ^{[4
]}

Tanaka, Hiroyuki ^{[4
]}

Fukumoto, Yoshihiro ^{[1
]}

机构：

[1] Kurume Univ, Dept Internal Med, Div Cardiovasc Med, Sch Med, Kurume, Fukuoka, Japan

[2] Kurume Univ, Cardiovasc Res Inst, 67 Asahimachi, Kurume, Fukuoka 8300011, Japan

[3] Int Univ Hlth & Welf, Fukuoka, Japan

[4] Kurume Univ, Dept Surg, Div Cardiovasc Surg, Sch Med, Kurume, Fukuoka, Japan

来源：

JACC-BASIC TO TRANSLATIONAL SCIENCE | 2020年 / 5卷 / 02期

关键词：

aortic dissection; inflammation; Jak/Stat; smooth muscle cells; INTERNATIONAL REGISTRY; ANGIOTENSIN-II; TENASCIN-C; EXPRESSION; PROLIFERATION; INFLAMMATION; FIBROBLAST; ANEURYSMS; INSIGHTS;

D O I：

10.1016/j.jacbts.2019.10.010

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Aortic dissection (AD) is the acute destruction of aortic wall and is reportedly induced by inflammatory response. Here we investigated the role of smooth muscle Socs3 (a negative regulator of Janus kinases/signal transducer and activator of transcription signaling) in AD pathogenesis using a mouse model generated via beta-aminopropionitrile and angiotensin II infusion. Socs3 deletion specifically in smooth muscle cells yielded a chronic inflammatory response of the aortic wall, which was associated with increased fibroblasts, reinforced aortic tensile strength, and less-severe tissue destruction. Although an acute inflammatory response is detrimental in AD, smooth muscle-regulated inflammatory response seemed protective against AD. (C) 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.

引用

页码：126 / 144

页数：19

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