Jan 18, 2011

Cell deformation at the air-liquid interface induces Ca2+-dependent ATP release from lung epithelial cells

American Journal of Physiology. Lung Cellular and Molecular Physiology
Ronaldo RamsinghRyszard Grygorczyk

Abstract

Extracellular nucleotides regulate mucociliary clearance in the airways and surfactant secretion in alveoli. Their release is exquisitely mechanosensitive and may be induced by stretch as well as airflow shear stress acting on lung epithelia. We hypothesized that, in addition, tension forces at the air-liquid interface (ALI) may contribute to mechanosensitive ATP release in the lungs. Local depletion of airway surface liquid, mucins, and surfactants, which normally protect epithelial surfaces, facilitate such release and trigger compensatory mucin and fluid secretion processes. In this study, human bronchial epithelial 16HBE14o(-) and alveolar A549 cells were subjected to tension forces at the ALI by passing an air bubble over the cell monolayer in a flow-through chamber, or by air exposure while tilting the cell culture dish. Such stimulation induced significant ATP release not involving cell lysis, as verified by ethidium bromide staining. Confocal fluorescence microscopy disclosed reversible cell deformation in the monolayer part in contact with the ALI. Fura 2 fluorescence imaging revealed transient intracellular Ca(2+) elevation evoked by the ALI, which did not entail nonspecific Ca(2+) influx from the extracellular space....Continue Reading

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Mentioned in this Paper

Pathologic Cytolysis
Ethylmaleimide
Bronchial System
Stress, Mechanical
Surfactant [EPC]
Endogenous Surfactants
Lung
Extracellular
Calcium
Mucin-1 protein

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