@文章{Harki2004518，作者= {Harki, Olfa and Tamisier, Renaud and P{\'e}pin, Jean-Louis and Bailly, S{\'e}bastien and Mahmani, Anissa and Gonthier, Brigitte and Salomon, Aude and Vilgrain, Isabelle and Faury, Gilles and Brian{\c}on-Marjollet, Anne}，标题= {VE-cadherin cleavage in sleep apnoea:关于间歇性缺氧相关内皮通透性的新见解}，volume = {58}， number ={4}，位置-id ={2004518}，年份= {2021}，doi ={10.1183/13993003.04518-2020}，出版商={欧洲呼吸学会}，摘要={背景阻塞性睡眠呼吸暂停(OSA)引起间歇性缺氧，进而诱导内皮功能障碍和动脉粥样硬化进展。188bet官网地址我们假设ve -钙粘蛋白裂解，通过其释放的细胞外片段溶于血液(sVE)检测，可能是出现异常内皮通透性的早期指标。我们的目的是评估VE-cadherin在OSA患者体内和体外间歇缺氧模型中的切割，以破译细胞机制和后果。方法对间歇性缺氧14晚的7名健康志愿者、43名OSA患者和31名健康对照组的血清中sVE含量进行分析。体外实验中，将人主动脉内皮细胞(HAECs)暴露于6小时的间歇性缺氧环境中，有或没有抗氧化剂或缺氧诱导因子(HIF)-1、酪氨酸激酶或血管内皮生长因子(VEGF)通路的抑制剂。评估ve -钙粘蛋白裂解和磷酸化，并通过测量跨内皮电阻(TEER)和异硫氰酸荧光素(FITC){\textendash}葡聚糖通量评估内皮通透性。结果间歇性缺氧健康志愿者和OSA患者治疗前血清sVE显著升高，而持续气道正压治疗6个月后血清sVE下降。在多变量分析中，OSA是导致sVE变化的主要因素。在体外实验中，VE-cadherin的切割和表达随着HAEC暴露于间歇性缺氧而增加。 TEER decreased and FITC{\textendash}dextran flux increased. These effects were reversed by all of the pharmacological inhibitors tested.Conclusions We suggest that in OSA, intermittent hypoxia increases endothelial permeability in OSA by inducing VE-cadherin cleavage through reactive oxygen species production, and activation of HIF-1, VEGF and tyrosine kinase pathways.This study demonstrates for the first time that VE-cadherin is cleaved in sleep apnoea patients, in volunteers exposed to 14 nights of intermittent hypoxia and in endothelial cells exposed to in vitro intermittent hypoxia, leading to increased endothelial permeability https://bit.ly/3sAy5sc}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/58/4/2004518}, eprint = {//www.qdcxjkg.com/content/58/4/2004518.full.pdf}, journal = {European Respiratory Journal} }