| First Author | Kirabo A | Year | 2011 |
| Journal | J Mol Cell Cardiol | Volume | 50 |
| Issue | 6 | Pages | 1026-34 |
| PubMed ID | 21420414 | Mgi Jnum | J:173798 |
| Mgi Id | MGI:5050372 | Doi | 10.1016/j.yjmcc.2011.03.005 |
| Citation | Kirabo A, et al. (2011) Vascular smooth muscle Jak2 deletion prevents angiotensin II-mediated neointima formation following injury in mice. J Mol Cell Cardiol 50(6):1026-34 |
| abstractText | 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 (AT(1)-R) resulting in enhanced cell growth. However, the role that Jak2 plays in AT(1)-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 alpha-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. |
