Cross talk between polysulfide and nitric oxide in rat peritoneal mast cells

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Date: June 2016
Publisher: American Physiological Society
Document Type: Author abstract; Report
Length: 263 words

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Abstract :

The aim of this study was to define the effects of polysulfide on intracellular [Ca.sup.2+] concentration ([[[Ca.sub.2+]].sub.i]) and the underlying machinery, especially from the hydrogen sulfide ([H.sub.2]S) and nitric oxide (NO) perspectives, in rat peritoneal mast cells. We found that a polysulfide donor, [Na.sub.2][S.sub.4], increased [[[Ca.sub.2+]].sub.i], which is both extracellular and intracellular [Ca.sup.2+] dependent. Intracellular [Ca.sup.2+] release induced by [Na.sub.2][S.sub.4] was attenuated by the addition of a ryanodine receptor blocker. A slow-releasing [H.sub.2]S donor, GYY4137, dose dependently increased [[[Ca2.sup.+]].sub.i] that was independent from extracellular [Ca.sup.2+] influx. The GYY4137-induced [[[Ca.sup.2+]].sub.i] release was partially attenuated in the presence of the ryanodine receptor blocker. Both polysulfide and [H.sub.2]S 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 [H.sub.2]S-donor-induced [[[Ca.sup.2+]].sub.i] elevation in the absence of extracellular [Ca.sup.2+]. An NO donor, diethylamine (DEA) NONOate, increased [[[Ca.sup.2+]].sub.i] in a concentration-dependent manner, in which both extracellular and intracellular [Ca.sup.2+] are associated. At higher concentrations, the DEA NONOate-induced [[[Ca.sup.2+]].sub.i] increases were attenuated in the absence of extracellular [Ca.sup.2+] and by the addition of the ryanodine receptor blocker. [H.sub.2]S and NO dose dependently induced polysulfide production. Curiously, polysulfide, [H.sub.2]S, and NO donors had no effect on mast cell degranulation. Among synthases, cystathionine-[gamma]-lyase, and neuronal NOS seemed to be the major [H.sub.2]S- and NO-producing synthases, respectively. These results indicate that polysulfide acts as a potential signaling molecule that regulates [[[Ca.sup.2+]].sub.i] homeostasis in rat peritoneal mast cells via a cross talk with NO and [H.sub.2]S. polysulfide; hydrogen sulfide; nitric oxide; [Ca.sup.2+]; mast cells doi: 10.1152/ajpcell.00028.2016.

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Gale Document Number: GALE|A457692918