Upregulation of BAD, a pro-apoptotic protein of the BCL2 family, in vascular smooth muscle cells exposed to uremic conditions

被引:32
作者
Trecherel, Eric [2 ]
Godin, Corinne [2 ]
Louandre, Christophe
Benchitrit, Joyce [2 ]
Poirot, Sabrina [2 ]
Maziere, Jean-Claude [2 ]
Massy, Ziad A. [2 ,3 ]
Galmiche, Antoine [1 ,2 ]
机构
[1] CHU Nord, INSERM, U1088, Biochim Lab, F-80054 Amiens, France
[2] Univ Picardie Jules Verne, INSERM, U1088, Fac Med, Amiens, France
[3] CHU Sud, Serv Pharmacol Clin & Nephrol, Amiens, France
关键词
Chronic kidney disease; Uremic toxins; BCL2; Apoptosis; Vascular smooth muscle cells; CHRONIC KIDNEY-DISEASE; ATHEROSCLEROSIS; CALCIFICATION;
D O I
10.1016/j.bbrc.2011.11.144
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic kidney disease (CKD) has recently emerged as a major risk factor for cardiovascular pathology. CKD patients display accelerated atherosclerotic process, leading to circulatory complications. However, it is currently not clear how uremic conditions accelerate atherosclerosis. Apoptosis is an important homeostatic regulator of vascular smooth cells under pathological conditions. In the present study, we explored the regulation of apoptosis in cells of the vascular wall in the uremic context. We analysed the expression and regulation of the proteins of the BCL2 family that play an essential role in apoptosis. Our results, obtained in mice and primary human smooth muscle cells exposed to two uremic toxins, point to the existence of an alteration in expression and function of one pro-apoptotic member of this family, the protein BAD. We explore the regulation of BAD by uremic toxins and report the sensitization of vascular smooth muscle cells to apoptosis upon BAD induction. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:479 / 483
页数:5
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