ty - jour t1 - 睡眠呼吸暂停中的山雀乳酪裂解：新的见解进入间歇性缺氧相关内皮渗透性jf - 欧洲呼吸杂志jo - eur reshir j do - 10.1183/13993003.04518-2020 vl - 58是 - 4 sp - 2004518 au -Harki，Olfa Au - Tamisier，雷尼·奥 - 巴林，Jean-Louis Au - Mahmani，Anissa Au - Gonthier，Brigitte Au - Salomon，Aude Au - vilgrain，Isabelle Au - Faury，Gilles Au - Briançon-Marjollet，安妮Y1 - 2021/10/01 UR - //www.qdcxjkg.com/content/58/4/2004518.abstract n2 - 背景阻塞性睡眠呼吸暂停（OSA）导致间歇性缺氧，又导致内皮功能障碍和动脉粥样硬化进展。我们假设由其血液（SVE）中溶解的释放细胞外片段检测到的Ve-Cadherin裂解，可能是出苗异常内皮渗透性的早期指标。我们的目的是评估OSA患者的Ve-Cadherin切割，体内患者和体外间歇性缺氧模型来破译细胞机制和后果。从七个健康志愿者的血清暴露于14晚的间歇性缺氧，43岁的患者和31例健康分析控制受试者的SVE含量。人的主动脉内皮细胞（HAECs）在体外暴露于6小时，有或没有缺氧诱导因子（HIF）-1，酪氨酸激酶或血管内皮生长因子（VEGF）途径的抗氧化剂或抑制剂。评价VE-CADHERIN裂解和磷酸化，通过测量颅胸电阻（TEER）和荧光素异硫氰酸酯（FITC） - 甲苯胺来评估内皮渗透性。结果在从提交给间歇性缺氧和OSA患者之前的健康志愿者血清显着升高。治疗，但在OSA患者的连续阳性气道压力处理6个月后相反减少。 OSA was the main factor accounting for sVE variations in a multivariate analysis. In in vitro experiments, cleavage and expression of VE-cadherin increased upon HAEC exposure to intermittent hypoxia. TEER decreased and FITC–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 ER -