Smooth muscle specific overexpression of p22phox potentiates carotid artery wall thickening in response to injury.
Smooth muscle specific overexpression of p22phox potentiates carotid artery wall thickening in response to injury.
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DOI：
10.1155/2015/305686
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发表时间：
2015
影响因子：
--
通讯作者：
Weber DS
中科院分区：
文献类型：
--
作者：
Manogue MR;Bennett JR;Holland DS;Choi CS;Drake DA;Taylor MS;Weber DS
我们假设，与野生型小鼠相比，在平滑肌中选择性过表达NADPH氧化酶p22phox亚基（Tgp22smc）的转基因小鼠对经腔颈动脉损伤的反应会加剧。为了研究活性氧（ROS）作为血管损伤介质的作用，通过测量Tgp22smc和野生型动物在损伤后第3、7和14天的损伤和未损伤动脉的壁厚度（WT）和横截壁面积（CSWA）来量化损伤反应。Akt、p38 MAPK和Src活化在相同的时间点使用蛋白质印迹法进行评估。WT和CSWA损伤后显着更大的Tgp 22 SMC小鼠在7和14天后损伤，而未受伤的对侧颈动脉组之间是相似的。夹竹桃麻素治疗减弱了两组的损伤反应，并使Tgp22smc小鼠和野生型小鼠之间的反应相似。损伤后，与野生型小鼠相比，Tgp22smc小鼠的颈动脉在第3天表现出Akt活化升高，而p38 MAPK和Src活化在第7天升高。在这种血管ROS升高的转基因模型中，这些信号通路的激活和时间调节的增加可能有助于增强血管生长以响应损伤。
We hypothesized that transgenic mice overexpressing the p22phox subunit of the NADPH oxidase selectively in smooth muscle (Tgp22smc) 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 both Tgp22smc 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 in Tgp22smc 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 between Tgp22smc mice and wild-type mice. Following injury, carotid arteries from Tgp22smc 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.
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影响因子：
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DOI：
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发表时间：
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影响因子：
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