Dietl Paul, Liss Birgit, Felder Edward, Miklavc Pika, Wirtz Hubert
Institute of General Physiology, University of Ulm, Ulm, Germany.
Cell Physiol Biochem. 2010;25(1):1-12. doi: 10.1159/000272046. Epub 2009 Dec 22.
A major function of the pulmonary alveolar type II cell is the secretion of surfactant, a lipoprotein-like substance, via exocytosis of secretory vesicles termed lamellar bodies (LBs). The process of surfactant secretion is remarkable in several aspects, considering stimulus-delayed fusion activity, poor solubility of vesicle contents, long hemifusion lifetimes, slow fusion pore expansion and active, actin-driven content release. Cell stretch as well as P2Y(2) receptor stimulation by extracellular ATP are considered the most potent stimuli for LB exocytosis. For both stimuli, elevation of the cytoplasmic Ca(2+) concentration Ca(2+) is a key step. This review summarizes possible physiological roles and pathways of stretch- or ATP-induced surfactant secretion and discusses molecular mechanisms controlling the pre-, hemi- and postfusion phase, in comparison with neuroendocrine release mechanisms.
肺泡II型细胞的一项主要功能是通过称为板层小体(LB)的分泌性囊泡的胞吐作用分泌表面活性剂,一种脂蛋白样物质。考虑到刺激延迟融合活性、囊泡内容物溶解性差、半融合寿命长、融合孔扩张缓慢以及肌动蛋白驱动的活性内容物释放,表面活性剂分泌过程在几个方面都很显著。细胞拉伸以及细胞外ATP对P2Y(2)受体的刺激被认为是LB胞吐作用最有效的刺激因素。对于这两种刺激,细胞质Ca(2+)浓度[Ca(2+)]c的升高是关键步骤。本综述总结了拉伸或ATP诱导的表面活性剂分泌的可能生理作用和途径,并与神经内分泌释放机制相比,讨论了控制融合前、半融合和融合后阶段的分子机制。