Genetic Deletion of Socs3 in Smooth Muscle Cells Ameliorates Aortic Dissection in Mice.
JACC Basic Transl Sci
; 5(2): 126-144, 2020 Feb.
Article
em En
| MEDLINE
| ID: mdl-32140621
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 ß-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.
AD, aortic dissection; AngII, angiotensin II; BAPN, ß-aminopropionitrile; ECM, extracellular matrix; IL, interleukin; Jak/Stat; Jnk, c-Jun N-terminal kinases; KO, knockout; Lox, lysyl oxidase; SM2, smooth muscle myosin heavy chain; SMA, smooth muscle α-actin; SMC, smooth muscle cell; SMemb, embryonic isoform of myosin heavy chain; Socs, suppressor of cytokine signaling; Stat, signal transducer and activator of transcription; WT, wild type; aortic dissection; inflammation; p, phosphorylated; smSocs3-KO, knockout of the smooth muscle cell Socs3; smooth muscle cells
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MEDLINE
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En
Ano de publicação:
2020
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Article