homeodomain interacting protein kinase 2 activation compromises endothelial cell response to laminar flow protective role of p21waf1,cip1,sdi1homeodomain交互激活蛋白激酶2妥协内皮细胞响应p21waf1层流保护作用,cip1 sdi1.pdfVIP

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2017-09-01 发布于上海
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homeodomain interacting protein kinase 2 activation compromises endothelial cell response to laminar flow protective role of p21waf1,cip1,sdi1homeodomain交互激活蛋白激酶2妥协内皮细胞响应p21waf1层流保护作用,cip1 sdi1.pdf

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homeodomain interacting protein kinase 2 activation compromises endothelial cell response to laminar flow protective role of p21waf1,cip1,sdi1homeodomain交互激活蛋白激酶2妥协内皮细胞响应p21waf1层流保护作用,cip1 sdi1

Homeodomain Interacting Protein Kinase 2 Activation Compromises Endothelial Cell Response to Laminar Flow: Protective Role of p21waf1,cip1,sdi1 1 2 1¤ 1 2 Stefania Mattiussi , Chiara Lazzari , Silvia Truffa , Annalisa Antonini , Silvia Soddu , Maurizio C. 1 1 Capogrossi , Carlo Gaetano * 1 Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’ Immacolata, Roma, Italy, 2 Laboratorio di Oncogenesi Molecolare, Dipartimento di Oncologia Sperimentale, Istituto Regina Elena, Roma, Italy Abstract Background: In the cardiovascular system, laminar shear stress (SS) is one of the most important source of endothelial protecting signals. Physical and chemical agents, however, including ionising radiations and anticancer drugs, may injure endothelial cells determining an increase in oxidative stress and genotoxic damage. Whether the SS protective function remains intact in the presence of strong oxidants or DNA damage is currently unclear. Methods and Results: To investigate this aspect a series of experiments were performed in which HUVEC were exposed to sub-lethal doses of the radio-mimetic compound Bleomycin (Bleo; 10 mg/ml) which generated free radicals (ROS) without significantly compromising cell survival. Remarkably, the application of a SS of 12 dyne/cm2 did not protect endothelial cells but markedly accelerated apoptosis compared to controls kept in static culture and in the presence of Bleo. Experiments with the inducible nitric oxide synthase (iNOS) inhibitor GW274150 significantly reduced the SS-dependent apoptosis indicating that the production of NO was relevant for this effect. At molecular level, the ataxia-telangectasia-mutated (ATM) kinase, the homeo