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Alteration of p66shc is associated with endothelial dysfunction in the abdominal aortic coarctation of rats
Author(s) -
Lee Sang Ki,
Kim Hyo Shin,
Song Yun Jeong,
Joo Hee Kyoung,
Lee Ji Young,
Lee Kwon Ho,
Cho Eun Jung,
Cho Chung-Hyun,
Park Jin Bong,
Jeon Byeong Hwa
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.06.026
Subject(s) - phosphorylation , endothelial dysfunction , nitric oxide , endothelium , medicine , endocrinology , angiotensin ii , acetylcholine , vasodilation , superoxide , chemistry , blood pressure , biochemistry , enzyme
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.