Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10872152 | FEBS Letters | 2008 | 6 Pages |
Abstract
To examine the role of p66shc in endothelial dysfunction, we investigated the endothelium-dependent relaxation, protein expression and superoxide production in abdominal aortic coarctation rats. Endothelium-dependent relaxation to acetylcholine was impaired only in the aortic segments above the aortic coarctation (35.0±7.1% vs. 86.6 ± 6.0% for sham control at 1 μM Ach). The aortic segments exposed to increased blood pressure showed a decreased phosphorylation of endothelial nitric oxide synthase, an increased phosphorylation of p66shc, and an increased superoxide production. Angiotensin II elicited a significantly increased phosphorylation of p66shc in the endothelial cells. Taken together, these findings suggest that the increased phosphorylation of p66shc is one of the important mediators in the impaired endothelium-dependent relaxation of aortic coarctation rats.
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Authors
Sang Ki Lee, Hyo Shin Kim, Yun Jeong Song, Hee Kyoung Joo, Ji Young Lee, Kwon Ho Lee, Eun Jung Cho, Chung-Hyun Cho, Jin Bong Park, Byeong Hwa Jeon,