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平滑肌细胞中 Socs3 的基因缺失改善了小鼠的主动脉夹层。

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

作者信息

Hirakata Saki, Aoki Hiroki, Ohno-Urabe Satoko, Nishihara Michihide, Furusho Aya, Nishida Norifumi, Ito Sohei, Hayashi Makiko, Yasukawa Hideo, Imaizumi Tsutomu, Hiromatsu Sinichi, Tanaka Hiroyuki, Fukumoto Yoshihiro

机构信息

Division of Cardiovascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.

Cardiovascular Research Institute, Kurume University, Kurume, Japan.

出版信息

JACC Basic Transl Sci. 2020 Jan 8;5(2):126-144. doi: 10.1016/j.jacbts.2019.10.010. eCollection 2020 Feb.

DOI:10.1016/j.jacbts.2019.10.010
PMID:32140621
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7046542/
Abstract

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 β-aminopropionitrile and angiotensin II infusion. 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.

摘要

主动脉夹层（AD）是主动脉壁的急性破坏，据报道是由炎症反应引起的。在这里，我们使用通过输注β-氨基丙腈和血管紧张素II生成的小鼠模型，研究了平滑肌中的细胞因子信号转导抑制因子3（Janus激酶/信号转导子和转录激活子信号的负调节因子）在AD发病机制中的作用。平滑肌细胞中的特异性缺失产生了主动脉壁的慢性炎症反应，这与成纤维细胞增加、主动脉抗张强度增强和组织破坏较轻有关。虽然急性炎症反应在AD中是有害的，但平滑肌调节的炎症反应似乎对AD具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/a8f77525ec80/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/10febe8cdbad/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/ceba993e1c4b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/d0cce9e4ebbb/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/ce0c5baa3fd3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/3580dc2863a4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/0c4399d5f335/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/e482c383408f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/2bd8c6da4a0d/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/a8f77525ec80/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/10febe8cdbad/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/ceba993e1c4b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/d0cce9e4ebbb/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/ce0c5baa3fd3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/3580dc2863a4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/0c4399d5f335/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/e482c383408f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/2bd8c6da4a0d/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8862/7046542/a8f77525ec80/gr8.jpg

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