@Article {Sun1900300，作者= {Sun，青竹和方，雷和罗斯，迈克尔和唐，Xuemei和Papakonstantinou，Eleni和Zhai，Weiqi和Louis，Renaud和Heinen，Vincent和Schleich，Florence N.和Lu，Shemin和Savic，Spasenjia和Tamm，Michael和Stolz，Daiana}，标题= {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}，体积= {54}，数量={6}，Elocation-ID = {1900300}，年= {2019}，DOI = {10.1183 / 13993003.00300-2019}，出版商= {欧洲呼吸社会}，摘要= {188bet官网地址支气管热塑术（BT）是迄今为止唯一的治疗这提供了气道墙重塑的持久减少。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。 BALF or Epi.S obtained after BT reduced the expression of C/EBPβ, ERK1/2, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α), PRMT1 and mitochondrial mass in airway fibroblasts. 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}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/54/6/1900300}, eprint = {//www.qdcxjkg.com/content/54/6/1900300.full.pdf}, journal = {European Respiratory Journal} }