Caspofungin induces the release of Ca2+ ions from internal stores by activating ryanodine receptor-dependent pathways in human tracheal epithelial cells.

Scientific Reports
Sabrina MüllerMichael Henrich

Abstract

The antimycotic drug caspofungin is known to alter the cell function of cardiomyocytes and the cilia-bearing cells of the tracheal epithelium. The objective of this study was to investigate the homeostasis of intracellular Ca2+ concentration ([Ca2+]i) after exposure to caspofungin in isolated human tracheal epithelial cells. The [Ca2+]i was measured using the ratiometric fluoroprobe FURA-2 AM. We recorded two groups of epithelial cells with distinct responses to caspofungin exposure, which demonstrated either a rapid transient rise in [Ca2+]i or a sustained elevation of [Ca2+]i. Both patterns of Ca2+ kinetics were still observed when an influx of transmembraneous Ca2+ ions was pharmacologically inhibited. Furthermore, in extracellular buffer solutions without Ca2+ ions, caspofungin exposure still evoked this characteristic rise in [Ca2+]i. To shed light on the origin of the Ca2+ ions responsible for the elevation in [Ca2+]i we investigated the possible intracellular storage of Ca2+ ions. The depletion of mitochondrial Ca2+ stores using 25 µM 2,4-dinitrophenol (DNP) did not prevent the caspofungin-induced rise in [Ca2+]i, which was rapid and transient. However, the application of caffeine (30 mM) to discharge Ca2+ ions that were...Continue Reading

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Citations

Nov 11, 2021·Journal of the European Academy of Dermatology and Venereology : JEADV·H ColbocS Ingen-Housz-Oro

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Methods Mentioned

BETA
Assay
Fluorescence

Software Mentioned

GraphPad PRISM
GraphPad

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