Expression and role of TASK-1 channels in pulmonary vessels and airways
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Abstract
TASK-1 is a member of the two pore domain K+ channel family. Its closing causes a decrease in K+ efflux, depolarization of cell membrane, opening of calcium channels and Ca2+ entry into the cell. This has been reported to occur under hypoxia while volatile anesthetics activate this channel. Consequently, TASK-1 may be involved in mechanisms of hypoxic pulmonary vasoconstriction (HPV) and anesthetics-induced inhibition of mucociliary clearance. In cell culture, the superoxide generating enzyme NOX4 has been considered as a functional partner of TASK-1 in O2 sensing. On this background, we set out to investigate in mice (1) the role of TASK-1 channel in HPV and bronchial constriction, (2) the functional relation between TASK-1 and NOX4 in sensing changes in O2 tension in pulmonary vessels, and (3) the role of TASK-1 in cilia driven particle transport on the tracheal mucosal surface.Link to publications or other datasets
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Giessen : VVB Laufersweiler