| First Author | Hou Y | Year | 2008 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 28 |
| Issue | 7 | Pages | 1257-62 |
| PubMed ID | 18436805 | Mgi Jnum | J:160044 |
| Mgi Id | MGI:4453296 | Doi | 10.1161/ATVBAHA.108.165688 |
| Citation | Hou Y, et al. (2008) Alpha2-antiplasmin is a critical regulator of angiotensin II-mediated vascular remodeling. Arterioscler Thromb Vasc Biol 28(7):1257-62 |
| abstractText | OBJECTIVE: Alpha2-antiplasmin (alpha2-AP) is the major circulating inhibitor of plasmin, which plays a determining role in the regulation of intravascular fibrinolysis. We investigated the role of alpha(2)-AP on vascular remodeling in response to angiotensin II (Ang II). METHODS AND RESULTS: alpha2-AP-deficient mice were performed. Ang II and N(omega)-nitro- L-arginine methyl ester (L-NAME)-induced perivascular fibrosis was significantly decreased in alpha2-AP-/- mice compared with wild-type mice. In situ gelatinolytic activity analysis shows that perivascular gelatinolytic activity was increased in alpha2-AP-/- mice, which was responsible for decreased perivascular fibrosis in response to Ang II and L-NAME. Ang II-induced arterial wall thickening, vascular cell proliferation, apoptosis, c-Myc, and collagen I expression were significantly decreased in alpha2-AP-/- mice compared with wild-type mice. Further analysis shows that increased p53 and p21 expression were responsible for inhibition of Ang II-induced vascular remodeling in alpha2-AP-/- mice. CONCLUSIONS: The results show that alpha2-AP is a critical regulator for vascular remodeling by inhibiting p53/p21 pathway, suggesting that alpha2-AP is proposed to be a potential therapeutic target for vascular remodeling. |
