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Disrupted eNOS activity and expression account for vasodilator dysfunction in different stage of sepsis.

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收录情况： ◇ SCIE ◇ 预警期刊

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机构： [1]Division of Cardiology, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China [2]Emergency Ward, The First People’s Hospital of Shangqiu, Henan 476000, China [3]Institute of Life Science, Chongqing Medical University, Chongqing 400016, China [4]Sichuan Academy of Chinese Medicine Science, Chengdu 610000, China [5]Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, 473 West 12th Avenue, Columbus, OH 43210, USA

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关键词： Endothelial dysfunction Endothelial nitric oxide synthase Sepsis

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Sepsis is a severe endothelial dysfunction syndrome. The role of endothelial nitric oxide synthase (eNOS) in endothelial dysfunction induced by sepsis is controversial. To explore the role of eNOS in vascular dysfunction. The effect of sepsis on vasodilation and eNOS levels was examined in septic mouse arteries and in cell models. In early sepsis mouse arteries, endothelium-dependent relaxation decreased and phosphorylation of the inhibitory Thr495 site in endothelial nitric oxide synthase increased. Mechanically, the phosphorylation of endothelial nitric oxide synthase at Thr497 in bovine aortic endothelial cells occurred in a protein kinase C-α dependent manner. In late sepsis, both nitric oxide-dependent relaxation responses and endothelial nitric oxide synthase levels were decreased in septic mice arteries. Endothelial nitric oxide synthase levels expression levels decreased in tumor necrosis factor-α-treated human umbilical vein endothelial cells and this could be prevented by the ubiquitin proteasome inhibitor (MG-132). MG-132 could reverse the decrease in endothelial nitric oxide synthase expression and improve nitric oxide-dependent vasodilator dysfunction in septic mice arteries. These data indicate that vasodilator dysfunction is induced by the increased phosphorylation of endothelial nitric oxide synthase in early sepsis and its degradation in late sepsis. Copyright © 2020 Elsevier Inc. All rights reserved.

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出版当年[2021]版：

大类 | 3 区医学

小类 | 3 区医学：研究与实验 3 区药学

最新[2023]版：

大类 | 2 区

医学

小类 | 2 区医学：研究与实验 2 区药学

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出版当年[2021]版：

Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q1 PHARMACOLOGY & PHARMACY

最新[2023]版：

Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q1 PHARMACOLOGY & PHARMACY

影响因子： 5.2 最新[2023版] 5.3 最新五年平均 6.78 出版当年[2021版] 6.044 出版当年五年平均 5.037 出版前一年[2020版] 6.1 出版后一年[2022版]

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第一作者机构： [1]Division of Cardiology, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China

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通讯机构： [1]Division of Cardiology, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China [3]Institute of Life Science, Chongqing Medical University, Chongqing 400016, China [5]Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, 473 West 12th Avenue, Columbus, OH 43210, USA [*1]The First Affiliated Hospital of Chongqing Medical University Division of Cardiology, Chongqing 400016, China. [*2]Medicine and Biochemistry, 394 BRT, The Ohio State University, 460 West 12th Avenue, Columbus, OH 43210, USA.

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