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|Title:||Effect of hydrogen sulfide on intracellular calcium homeostasis in neuronal cells||Authors:||Yong, Q.C.
|Keywords:||L-type calcium channel
T-type calcium channel
|Issue Date:||2010||Citation:||Yong, Q.C., Choo, C.H., Tan, B.H., Low, C.-M., Bian, J.-S. (2010). Effect of hydrogen sulfide on intracellular calcium homeostasis in neuronal cells. Neurochemistry International 56 (3) : 508-515. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neuint.2009.12.011||Abstract:||Hydrogen sulfide (H2S) is now known as a new biological mediator. In the present study, the effects of H2S on intracellular calcium ([Ca2+]i) in neuronal SH-SY5Y cells was investigated. In SH-SY5Y neuronal cells, NaHS, a H2S donor, concentration-dependently increased [Ca2+]i. The H2S-induced Ca2+ elevation was significantly attenuated by EGTA-treated calcium-free Krebs' solution. This elevation was also reduced by antagonists of L-type (verapamil and nifedipine), T-type (mibefradil) calcium channels and N-methyl-d-aspartate receptor (MK-801, AP-5 and ifenprodil). A 90% reduction in H2S-induced [Ca2+]i elevation was found in cells pretreated with combination of all three kinds of inhibitors. Depletion of intracellular Ca2+ store with thapsigargin or cyclopiazonic acid or blockade of ryanodine receptor with ruthenium red significantly attenuated the effect of H2S on [Ca2+]i. Inhibition of protein kinase A (PKA), phospholipase C (PLC) and protein kinase C (PKC) suppressed the H2S-elevated [Ca2+]i, suggesting that H2S may regulate [Ca2+]i via both PKA and PLC/PKC pathways. In conclusion, it was found in this study that H2S increased [Ca2+]i in SH-SY5Y neuronal cells by increasing Ca2+ influx via plasma membrane and in turn releasing calcium from intracellular calcium store. The findings in the present study provide the direct evidence that H2S may serve as a neuromodulator. © 2009 Elsevier Ltd.||Source Title:||Neurochemistry International||URI:||http://scholarbank.nus.edu.sg/handle/10635/27214||ISSN:||01970186||DOI:||10.1016/j.neuint.2009.12.011|
|Appears in Collections:||Staff Publications|
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