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Aim:To investigate the underlying mechanism of acid-sensing ion channel (ASIC)la involved in the acidosis-induced cytotoxicity of rat C6 glioma cells.Methods:The stable ASIC 1 a-silenced C6 cells built with the RNA interference technologywere confirmed by RT-PCR and Western blot analysis.Intracellular calcium([Ca~(2+)]_i) in both the wild-type rat C6 glioma cells and the ASIC 1a-silenced C6 cellswere analyzed before and after acid application/exposure with the calcium imagingexperiment.Results:The rapid extracellular pH drop induced the increase of[Ca~(2+)]_i in the wild-type C6 cells,but not in the ASIC1a-silenced C6 cells.Duringthe prolonged acid exposure,[Ca~(2+)]_i was lower in the ASIC 1 a-silenced C6 cellsthan that in the control cells.Conclusion:The resultant toxicity of [Ca~(2+)]_i mightcontribute to the acidosis-induced cytotoxicity.
Aim: To investigate the underlying mechanism of acid-sensing ion channel (ASIC) la involved in the acidosis-induced cytotoxicity of rat C6 glioma cells. Methods: The stable ASIC 1 a-silenced C6 cells built with the RNA interference technology wererefined by RT -PCR and Western blot analysis. Intracellular calcium ([Ca ~ (2 +)] _i) both in the wild-type rat C6 glioma cells and the ASIC 1a-silenced C6 cellswere analyzed before and after acid application / exposure with the calcium imagingexperiment .Results: The rapid extracellular pH drop induced the increase of [Ca ~ (2 +)] _i in the wild-type C6 cells, but not in ASIC1a-silenced C6 cells. During the prolonged acid exposure, [Ca ~ (2+ )] _i was lower in the ASIC 1 a-silenced C6 cell stop that in the control cells. Contact: The resultant toxicity of [Ca ~ (2 +)] _i might Contribute to the acidosis-induced cytotoxicity.