PT -期刊文章盟Harki Olfa盟——Tamisier Renaud盟——Pepin jean - louis AU -贝利Sebastien盟——Mahmani Anissa盟——Gonthier林盟-所罗门,这是盟——Vilgrain,伊莎贝尔盟——Faury Gilles盟——Briancon-Marjollet安妮TI - VE-cadherin乳沟在睡眠呼吸暂停:洞察间歇hypoxia-related内皮渗透性援助- 10.1183/13993003.04518 -2020 DP - 2021年10月01 TA -欧洲呼吸杂志》第六PG - 2004518 - 58 IP - 4 4099 - //www.qdcxjkg.com/content/58/4/2004518.short 4100 - //www.qdcxjkg.com/content/58/4/2004518.full所以欧元和J2021 10月01;58 AB -背景阻塞性睡眠呼吸暂停(OSA)导致间歇性缺氧,进而诱发内皮功能障碍和动脉粥样硬化进展。我们提出VE-cadherin乳沟,血液中检测到其细胞外释放片段水溶性(sVE),可能是一个紧急内皮通透性异常的早期指标。我们的目的是评估VE-cadherin乳沟阻塞性睡眠呼吸暂停患者的体内和体外间歇缺氧模型来解释细胞机制和后果。方法从七个健康志愿者血清暴露于14晚的间歇性缺氧,43阻塞性睡眠呼吸暂停综合症患者和健康对照组31日sVE内容进行分析。人类主动脉内皮细胞(HAECs)暴露在6 h(体外间歇缺氧,有或没有抗氧化剂或低氧诱导因子(HIF)抑制剂1,酪氨酸激酶或血管内皮生长因子(VEGF)的途径。内皮渗透性VE-cadherin乳沟和磷酸化进行评估,评估通过测量transendothelial电阻(te)和异硫氰酸荧光素(FITC)右旋糖酐通量。结果sVE显著升高血清中健康志愿者提交间歇性缺氧和阻塞性睡眠呼吸暂停综合症患者在治疗之前,但反过来降低阻塞性睡眠呼吸暂停患者的6个月后持续正压通气治疗。阻塞性睡眠呼吸暂停综合症的主要因素是占sVE多元分析的变化。在体外实验中,乳沟和表达VE-cadherin增加HAEC间歇性缺氧。 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