title: Cross talk between polysulfide and nitric oxide in rat peritoneal mast cells.
abstract: The aim of this study was to define the effects of polysulfide on intracellular Ca(2+) concentration ([Ca(2+)]i) and the underlying machinery, especially from the hydrogen sulfide (H2S) and nitric oxide (NO) perspectives, in rat peritoneal mast cells. We found that a polysulfide donor, Na2S4, increased [Ca(2+)]i, which is both extracellular and intracellular Ca(2+) dependent. Intracellular Ca(2+) release induced by Na2S4 was attenuated by the addition of a ryanodine receptor blocker. A slow-releasing H2S donor, GYY4137, dose dependently increased [Ca(2+)]i that was independent from extracellular Ca(2+) influx. The GYY4137-induced [Ca(2+)]i release was partially attenuated in the presence of the ryanodine receptor blocker. Both polysulfide and H2S donors increased the intracellular NO levels in DAF-2-loaded mast cells, which were abolished by an NO scavenger, cPTIO. Inhibition of NO synthase (NOS) significantly abolished the polysulfide- or H2S-donor-induced [Ca(2+)]i elevation in the absence of extracellular Ca(2+) An NO donor, diethylamine (DEA) NONOate, increased [Ca(2+)]i in a concentration-dependent manner, in which both extracellular and intracellular Ca(2+) are associated. At higher concentrations, the DEA NONOate-induced [Ca(2+)]i increases were attenuated in the absence of extracellular Ca(2+) and by the addition of the ryanodine receptor blocker. H2S and NO dose dependently induced polysulfide production. Curiously, polysulfide, H2S, and NO donors had no effect on mast cell degranulation. Among synthases, cystathionine-γ-lyase, and neuronal NOS seemed to be the major H2S- and NO-producing synthases, respectively. These results indicate that polysulfide acts as a potential signaling molecule that regulates [Ca(2+)]i homeostasis in rat peritoneal mast cells via a cross talk with NO and H2S.
authors.affiliation: Laboratory of Physiology, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan; and Department of Physiology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Amira
authors.initials: A
authors.lastname: Moustafa
authors.affiliation: Laboratory of Physiology, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan; and habara@vetmed.hokudai.ac.jp.
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Habara
mesh_terms: D000818:Animals; D020013:Calcium Signaling / Q000187:drug effects; D004789:Enzyme Activation; D006706:Homeostasis; D006834:Hydrazines / Q000494:pharmacology; D006862:Hydrogen Sulfide / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism*; D009025:Morpholines / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D009946:Organothiophosphorus Compounds / Q000494:pharmacology; D010537:Peritoneum / Q000166:cytology*; D017208:Rats, Wistar; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D017670:Sodium Compounds / Q000378:metabolism / Q000494:pharmacology; D013440:Sulfides / Q000378:metabolism* / Q000494:pharmacology; D013997:Time Factors
chemical_list: C529376:GYY 4137; D006834:Hydrazines; D009025:Morpholines; D020030:Nitric Oxide Donors; D009946:Organothiophosphorus Compounds; D019837:Ryanodine Receptor Calcium Release Channel; D017670:Sodium Compounds; D013440:Sulfides; C519323:sodium tetrasulfide; D009569:Nitric Oxide; C084012:1,1-diethyl-2-hydroxy-2-nitrosohydrazine; C032915:polysulfide; D019001:Nitric Oxide Synthase; D006862:Hydrogen Sulfide
keywords: Ca2+; hydrogen sulfide; mast cells; nitric oxide; polysulfide