Ty -jour t1-囊性纤维化中的高血糖影响BK通道的不利影响粘液清除JF的功能 - 欧洲呼吸杂志JO -EUR RESSIR J DO -10.1183/13993003.00503.00509-2020 VL -57。/01 ur-http：//www.qdcxjkg.com/content/57/1/1/2000509.Abstract N2-大conductance，CA2+激活，电压 - 依赖性K+（BK）通道功能对于适当的气道水合和粘液级水分至关重要功能。在气道上皮中，BK功能受其γ-亚基，富含亮氨酸重复的蛋白26（LRRC26）调节。由于囊性纤维化（CF）相关的糖尿病（CFRD）患者的肺功能结果较差，因此这项研究确定了高血糖对BK功能在CF支气管上皮（CFBE）细胞中的影响，并在体外评估了Glycemciporsions apcursions和mRNA的相关性LRC26在CF和CFRD患者的上呼吸道中的表达。CFBE细胞在含有5.5 mm或12.5 mm葡萄糖的培养基中在空气 - 液界面（ALI）处重新分化。BK活性是在USSing室中测量的。通过半月板扫描估算气道表面液体（ASL）体积，并通过定量实时PCR和酶联免疫吸附测定法（ELISA）测量炎症标记表达。通过连续葡萄糖监测（CGM）进行7天的7天评估CF患者。通过在葡萄糖监测结束时获得的鼻细胞的定量实时PCR测量LRRC26 mRNA表达。在高葡萄糖下培养的CFBE细胞中，B电流显着降低。 These cells revealed significantly lower ASL volumes and increased inflammation, including the receptor for advanced glycation endproducts (RAGE), compared to cells cultured in normal glucose. In vivo, nasal cell expression of LRRC26 mRNA was inversely correlated with hyperglycaemic excursions, consistent with the in vitro results.Our findings demonstrate that hyperglycaemia induces inflammation and impairs BK channel function in CFBE cells in vitro. These data suggest that declining lung function in CFRD patients may be related to BK channel dysfunction.In CF patients, hyperglycaemia downregulates airway epithelial BK channels that are critical for mucociliary clearance. Mechanistically, hyperglycaemia suppresses expression of the BK γ-subunit LRRC26, which is required for its function in the airway. https://bit.ly/315FCTV ER -