PT - 杂志 - 日志Au - Sun，青柱Au - 方，雷奥 - 罗斯，迈克尔Au - 唐，Xuemei Au - Papakonstantinou，Eleni Au - Zhai，Weiqi Au - Louis，Renaud Au - Heinen，Vincent Au - Schleich，佛罗伦萨N。Au - Lu，Shemin Au-Savic，Spasenjia Au - Tamm，Michael Au - Stolz，Daiana Ti - 支气管热成形术通过阻断上皮衍生的热休克蛋白-60分泌物和蛋白质精氨酸甲基转移酶-1，在成纤维细胞助剂中降低了气道重塑 - 10.1183/13993003.00300-2019 DP - 2019年12月01日 - 欧洲呼吸期刊PG - 1900300 VI - 54 IP - 6 4099 - //www.qdcxjkg.com/content/54/6/1900300.short 4100 - http：//www.qdcxjkg.com/content/54/6/1900300.full so - 欧元reshir J2019 12月01日;54 AB - 支气管热塑术（BT）是迄今为止唯一提供持久减少气道墙体重塑的疗法。然而，BT的作用机制尚不清楚。该研究旨在表征重塑调节信号传导途径的变化，在哮喘中的哮喘。血糖血液（BALF）是从BT之前和之后的八个严重哮喘的患者获得。在（n = 66）之前和（n = 62）bt之前，从23名患者中分离出原发性支气管上皮细胞。收集上皮细胞培养上清液（EPI.S）并施用于原发性成纤维细胞。与在BT之前获得的上皮细胞相比，从哮喘患者获得的哮喘患者获得的初步细胞。在气道成纤维细胞中，BALF或ePI.S获得，在BT增加CCAAT增强剂结合蛋白-β（C /EBPβ）表达之前，从而下调MicroRNA-19a。这种上调的细胞外信号调节激酶-1 / 2（ERK1 / 2）表达，蛋白质精氨酸甲基转移酶-1（PRMT1）表达，细胞增殖和线粒体质量。BT在BT后获得的BALF或EPI。在气道成纤维细胞中降低C /EBPβ，ERK1 / 2，过氧化物体增殖物激活的受体-γ共粘膜剂-1α（PGC1α），PRMT1和线粒体质量的表达。 Proteome and transcriptome analyses indicated that epithelial cell-derived heat shock protein-60 (HSP60) is the main mediator of BT effects on fibroblasts. Further analysis suggested that HSP60 regulated PRMT1 expression, which was responsible for the increased mitochondrial mass and α-smooth muscle actin expression by asthmatic fibroblasts. These effects were ablated after BT. These results imply that BT reduces fibroblast remodelling through modifying the function of epithelial cells, especially by reducing HSP60 secretion and subsequent signalling pathways that regulate PRMT1 expression.We therefore hypothesise that BT decreases airway remodelling by blocking epithelium-derived HSP60 secretion and PRMT1 in fibroblasts.Bronchial thermoplasty reduces asthma-associated airway wall remodelling by epithelial cell-controlled downregulation of PRMT1 expression in fibroblasts http://bit.ly/2TLhCkC