Smooth Muscle Specific Overexpression of p22phox Potentiates Carotid Artery Wall Thickening in Response to Injury. (5th April 2015)

• Record Type: Journal Article
• Authors: Manogue, Michael R.; Bennett, Justin R.; Holland, Drury S.; Choi, Chung-Sik; Drake, Douglas A.; Taylor, Mark S.; Weber, David S.
• Other Names: Mouithys-Mickalad Ange Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2015(2015)
• Publication Date: 2015-04-05
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2015/305686
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : We hypothesized that transgenic mice overexpressing thep22 phox subunit of the NADPH oxidase selectively in smooth muscle (Tg p22smc ) would exhibit an exacerbated response to transluminal carotid injury compared to wild-type mice. To examine the role of reactive oxygen species (ROS) as a mediator of vascular injury, the injury response was quantified by measuring wall thickness (WT) and cross-sectional wall area (CSWA) of the injured and noninjured arteries in bothTg p22smc and wild-type animals at days 3, 7, and 14 after injury. Akt, p38 MAPK, and Src activation were evaluated at the same time points using Western blotting. WT and CSWA following injury were significantly greater inTg p22smc mice at both 7 and 14 days after injury while noninjured contralateral carotids were similar between groups. Apocynin treatment attenuated the injury response in both groups and rendered the response similar betweenTg p22smc mice and wild-type mice. Following injury, carotid arteries fromTg p22smc mice demonstrated elevated activation of Akt at day 3, while p38 MAPK and Src activation was elevated at day 7 compared to wild-type mice. Both increased activation and temporal regulation of these signaling pathways may contribute to enhanced vascular growth in response to injury in this transgenic model of elevated vascular ROS.