Author | Peyton, Kelly J. | en_US |
Author | Ensenat, Diana | en_US |
Author | Azam, Mohammad A. | en_US |
Author | Keswani, Amit N. | en_US |
Author | Kannan, Sankaranarayanan | en_US |
Author | Liu, Xiao-Ming | en_US |
Author | Wang, Hong | en_US |
Author | Tulis, David A. | en_US |
Author | Durante, William | en_US |
Date Accessioned | 2011-04-26T19:59:31Z | en_US |
Date Accessioned | 2011-05-17T00:56:27Z | |
Date Available | 2011-04-26T19:59:31Z | en_US |
Date Available | 2011-05-17T00:56:27Z | |
Date of Issue | 2009-04 | en_US |
Identifier (Citation) | Arteriosclerosis, Thrombosis, and Vascular Biology; 29:4 p. 488-494 | en_US |
Identifier (URI) | http://hdl.handle.net/10342/3371 | en_US |
Description | Objective—Arginase stimulates the proliferation of cultured vascular smooth muscle cells
(VSMCs); however, the influence of arginase on VSMC growth in vivo is not known. This study
investigated the impact of arginase on cell cycle progression and neointima formation following
experimental arterial injury.
Methods and Results—Balloon injury of rat carotid arteries resulted in a sustained increase in
arginase activity in the vessel wall and the induction of arginase I protein in both the media and
neointima of injured vessels. Furthermore, local perivascular application of the potent and selective
arginase inhibitors S-(2-boronoethyl)-L-cysteine (BEC) or NG-hydroxy-nor-L-arginine (L-OHNA)
immediately after injury markedly attenuated medial and neointimal DNA synthesis and neointima
formation. Substantial arginase I protein and arginase activity was also detected in rat cultured aortic
VSMCs. Moreover, treatment of VSMCs with BEC or L-OHNA, or knockdown of arginase I protein,
arrested cells in the G0/G1 phase of the cell cycle and induced the expression of the cyclin-dependent
protein kinase inhibitor, p21.
Conclusion—This study demonstrates that arginase is essential for VSMCs to enter the cell cycle
and that arginase I contributes to the remodeling response following arterial injury. Arginase I
represents a potentially new therapeutic target for the treatment of vasculoproliferative disorders.Originally published Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 29, No. 4, Apr 2009 | en_US |
Language | en_US | en_US |
Publisher | East Carolina University | en_US |
Related URI | http://atvb.ahajournals.org/cgi/content/full/29/4/488 | en_US |
Rights | Author was notified of opt-out rights by Cammie Jennings prior to upload of this article. | en_US |
Subject | Arginase | en_US |
Subject | Vascular smooth muscle cell poliferation | en_US |
Subject | Neointima | en_US |
Title | Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries | en_US |
Type | Article | en_US |
Identifier (PMID) | PMC2662760 | en_US |
Identifier (DOI) | 10.1161/ATVBAHA.108.183392 | |
Journal Name | Arteriosclerosis, Thrombosis, and Vascular Biology | |
Journal Volume | 29 | |
Journal Issue | 4 | |
Article Pages | 488-494 | |