Vascular smooth muscle Jak2 deletion prevents angiotensin II-mediated neointima formation following injury in mice

Annet Kirabo, S. Paul Oh, Hideko Kasahara, Kay Uwe Wagner, Peter P. Sayeski

Research output: Contribution to journalArticle

14 Scopus citations


The in vitro treatment of vascular smooth muscle cells (VSMC) with angiotensin II (Ang II) causes Janus kinase 2 (Jak2) to interact with the Ang II type 1 receptor (AT1-R) resulting in enhanced cell growth. However, the role that Jak2 plays in AT1-R-mediated vascular cell growth and remodeling in vivo is less clear. We hypothesized that in vivo, Jak2 plays a rate-limiting role in Ang II-mediated neointima formation following vascular injury. Using the Cre-loxP system, we conditionally ablated Jak2 from the VSMC of mice. We found that these mice are protected from Ang II-mediated neointima formation following iron chloride-induced vascular injury. In addition, the VSMC Jak2 null mice were protected from injury-induced vascular fibrosis and the pathological loss of the contractile marker, smooth muscle α-actin. Finally, when compared to controls, the VSMC Jak2 null mice exhibited significantly less Ang II-induced VSMC proliferation and migration in vitro and in vivo and more apoptosis. These results suggest that Jak2 plays a central role in the causation of Ang II-induced neointima formation following vascular injury and may provide a novel target for the prevention of neointima formation.

Original languageEnglish (US)
Pages (from-to)1026-1034
Number of pages9
JournalJournal of Molecular and Cellular Cardiology
Issue number6
StatePublished - Jun 1 2011



  • Angiotensin II
  • Jak2
  • Neointima
  • Vascular injury
  • Vascular smooth muscle cells

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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