Pharmacology · 2014
A comparison of the effects of nifedipine, verapamil, and low-molecular-weight heparin on SLIGRL-NH₂-induced calcium influx through proteinase-activated receptor 2 activation.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Sun Jun, Dou Wei, Shen Hong, Hu Jinhong
Аннотация
BACKGROUND: Proteinase-activated receptor 2 (PAR2) may be implicated in skin disorders. Intracellular calcium mobilization is a key step in PAR2-induced signaling.
AIMS: In this study, we investigated the effects of nifedipine, verapamil, and low-molecular-weight heparin (LMWH) on SLIGRL-NH₂-induced PAR2-mediated calcium mobilization within cells.
METHODS: The intracellular calcium concentration was measured with fluo-8, a fluorescence indicator for free Ca(2+).
RESULTS: Our results showed that SLIGRL-NH₂ induced a dose-dependent calcium influx. This calcium influx was completely blocked in HaCaT cells and significantly blocked by LMWH in HEK293/PAR2 cells. However, both nifedipine and verapamil failed to inhibit the SLIGRL-NH₂-induced calcium influx in either cell line.
CONCLUSION: These results indicate that the PAR2 activation-induced calcium mobilization was mediated by intracellular calcium stores but not by extracellular calcium present in the media.
AIMS: In this study, we investigated the effects of nifedipine, verapamil, and low-molecular-weight heparin (LMWH) on SLIGRL-NH₂-induced PAR2-mediated calcium mobilization within cells.
METHODS: The intracellular calcium concentration was measured with fluo-8, a fluorescence indicator for free Ca(2+).
RESULTS: Our results showed that SLIGRL-NH₂ induced a dose-dependent calcium influx. This calcium influx was completely blocked in HaCaT cells and significantly blocked by LMWH in HEK293/PAR2 cells. However, both nifedipine and verapamil failed to inhibit the SLIGRL-NH₂-induced calcium influx in either cell line.
CONCLUSION: These results indicate that the PAR2 activation-induced calcium mobilization was mediated by intracellular calcium stores but not by extracellular calcium present in the media.