Caspofungin induces the release of Ca2+ ions from internal stores by activating ryanodine receptor-dependent pathways in human tracheal epithelial cells
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...
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| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
16 July 2020
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| In: |
Scientific reports
Year: 2020, Jahrgang: 10 |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-020-68626-7 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/s41598-020-68626-7 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/s41598-020-68626-7 
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| Verfasserangaben: | Sabrina Müller, Christian Koch, Sebastian Weiterer, Markus A. Weigand, Michael Sander & Michael Henrich |
MARC
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| 520 | |a 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 presumably stored in the endoplasmic reticulum (ER) prior to caspofungin exposure completely inhibited the caspofungin-induced changes in [Ca2+]i levels. When the ER-bound IP3 receptors were blocked by 2-APB (40 µM), we observed a delayed transient rise in [Ca2+]i as a response to the caspofungin. Inhibition of the ryanodine receptors (RyR) using 40 µM ryanodine completely prevented the caspofungin-induced elevation of [Ca2+]i. In summary, caspofungin has been shown to trigger an increase in [Ca2+]i independent from extracellular Ca2+ ions by liberating the Ca2+ ions stored in the ER, mainly via a RyR pathway. | ||
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