2024-03-28T20:20:15Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/838302022-11-17T02:08:08Zhdl_2115_20048hdl_2115_140Hydrogen sulfide induces Ca2+ release from the endoplasmic reticulum and suppresses ATP-induced Ca2+ signaling in rat spinal cord astrocytesNii, TakeshiEguchi, RyotaYamaguchi, Soichiro1000040344494Otsuguro, Ken-ichiopen access© 2021. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 InternationalHydrogen sulfideATPCalciumAstrocytes649Hydrogen sulfide (H2S) has a variety of physiological functions. H2S reportedly increases intracellular Ca2+ concentration ([Ca2+];) in astrocytes. However, the precise mechanism and functional role of this increase are not known. Here, we examined the effects of H2S on [Ca2+]; in astrocytes from the rat spinal cord and whether H2S affects ATP-induced Ca2+ signaling, which is known to be involved in synaptic function. Na2S (150 mu M), an H2S donor, produced a nontoxic increase in [Ca2+];. The [Ca2+]; increase by Na2S was inhibited by Ca2+ depletion in the endoplasmic reticulum (ER) but not by removal of extracellular Ca2+, indicating that H2S releases Ca2+ from the ER. On the other hand, (NaS)-S-2 inhibited ATP-induced [Ca2+]; increase when Na2S clearly increased [Ca2+]; in the astrocytes, which was not suppressed by a reducing agent. In addition, Na2S had no effect on intracellular cyclic AMP (cAMP) level. These results indicate that oxidative post-translational modification of proteins and cAMP are not involved in the inhibitory effect of H2S on ATP-induced Ca2+ signaling. We conclude that H2S indirectly inhibits ATP-induced Ca2+ signaling by decreasing Ca2+ content in the ER in astrocytes. In this way, H2S may influence intercellular communication between astrocytes and neurons, thereby contributing to neuronal signaling in the nervous system.Elsevier2021-01-15engjournal articleAMhttp://hdl.handle.net/2115/83830https://doi.org/10.1016/j.ejphar.2020.1736840014-2999European journal of pharmacology891173684https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/83830/1/manuscript.pdfapplication/pdf652.87 KB2021-01-15