JACC: Basic to Translational Science (Feb 2020)

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

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

Journal volume & issue
Vol. 5, no. 2
pp. 126 – 144

Abstract

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Summary: 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. 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. Key Words: aortic dissection, inflammation, Jak/Stat, smooth muscle cells