Ribeiro Carla M P
Department of Medicine, Cystic Fibrosis/Pulmonary Research and Treatment Center, The University of North Carolina, Chapel Hill, NC 27599-7248, USA.
Methods Mol Biol. 2011;742:113-26. doi: 10.1007/978-1-61779-120-8_7.
The airways are continuously challenged by a variety of stimuli including bacteria, viruses, allergens, and inflammatory factors that act as agonists for G protein-coupled receptors (GPCR). Intracellular calcium (Ca(2+) (i)) mobilization in airway epithelia in response to extracellular stimuli regulates key airway innate defense functions, e.g., Ca(2+)-activated Cl(-) secretion, ciliary beating, mucin secretion, and inflammatory responses. Because Ca(2+) (i) mobilization in response to luminal stimuli is larger in CF vs. normal human airway epithelia, alterations in Ca(2+) (i) signals have been associated with the pathogenesis of CF airway disease. Hence, assessment of Ca(2+) (i) signaling has become an important area of CF research. This chapter will focus on measurements of cytoplasmic and mitochondrial Ca(2+) signals resulting from GPCR activation in polarized primary cultures of normal and CF human bronchial epithelia (HBE).
气道不断受到多种刺激的挑战，这些刺激包括细菌、病毒、过敏原和炎症因子，它们作为G蛋白偶联受体（GPCR）的激动剂。气道上皮细胞对细胞外刺激作出反应时的细胞内钙（Ca(2+) (i)）动员调节关键的气道固有防御功能，例如Ca(2+)激活的Cl(-)分泌、纤毛摆动、粘蛋白分泌和炎症反应。由于与正常人气道上皮相比，囊性纤维化（CF）患者气道上皮对腔内刺激的Ca(2+) (i)动员更大，Ca(2+) (i)信号的改变与CF气道疾病的发病机制有关。因此，评估Ca(2+) (i)信号已成为CF研究的一个重要领域。本章将重点介绍在正常人和CF患者人支气管上皮（HBE）的极化原代培养物中，由GPCR激活产生的细胞质和线粒体Ca(2+)信号的测量。
