ty -jour t1-睡眠呼吸暂停中的VE-钙粘蛋白裂解：与间歇性缺氧相关的内皮通透性JF的新见解JF-欧洲呼吸杂志Harki, Olfa AU - Tamisier, Renaud AU - Pépin, Jean-Louis AU - Bailly, Sébastien AU - Mahmani, Anissa AU - Gonthier, Brigitte AU - Salomon, Aude AU - Vilgrain, Isabelle AU - Faury, Gilles AU - Briançon-Marjollet，Anne Y1-2021/10/01 UR -http：//www.qdcxjkg.com/content/58/4/4/2004518.Abstract N2-背景阻塞性睡眠呼吸呼吸暂停（OSA）导致间歇性缺氧导致内皮功能障碍和Athephialial功能障碍，进展。我们假设VE-钙粘着蛋白的裂解是通过释放的细胞外碎片（SVE）释放的细胞外片段（SVE）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OSA患者以及体内和体外间歇性缺氧模型的VE-钙粘蛋白裂解，以破译细胞机制和后果。从7名健康志愿者中使用的血清，暴露于14晚的14晚间歇性低氧病人，43例OSA患者和31位健康的健康志愿者和43个健康的健康志愿者。分析了对照对象的SVE含量。人主动脉内皮细胞（HAEC）暴露于体外间歇性缺氧的6小时，有或没有缺氧诱导因子（HIF）-1的抗氧化剂或抑制剂-1，酪氨酸激酶或血管内皮内皮生长因子（VEGGF）途径。评估了Ve-钙粘着蛋白的裂解和磷酸化，并通过测量跨内皮电阻（TEER）和荧光素异硫氰酸酯（FITC） - DEXTRAN FLUXS VER.RESTS SVE评估内皮通透性。治疗，但在6个月的持续气道压力治疗后6个月后，OSA患者的治疗减少。 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 -