Role of the cytoskeleton in Ca2+ release from the intracellular Ca store of rat peritoneal mast cells

1991 ◽  
Vol 33 (1-2) ◽  
pp. 44-47 ◽  
Author(s):  
K. Tasaka ◽  
M. Mio ◽  
M. Akagi ◽  
K. Fujisawa ◽  
I. Aoki
2001 ◽  
Vol 425 (3) ◽  
pp. 229-238 ◽  
Author(s):  
Kheng H. Peh ◽  
Andrew Moulson ◽  
Beatrice Y.C. Wan ◽  
El-Sayed K. Assem ◽  
Frederick L. Pearce

1979 ◽  
Vol 178 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Shamshad Cockcroft ◽  
Bastien D. Gomperts

Histamine secretion and phosphatidylinositol turnover were compared in antigen-sensitized rat peritoneal mast cells stimulated with a number of different ligands. A small and variable increase in the incorporation of [32P]Pi and of [3H]inositol into phosphatidylinositol was observed when the cells were treated with immunoglobulin E-directed ligands (antigens and concanavalin A), and this was accompanied by a low amount of secretion (<10% of total cell histamine). In the presence of added phosphatidylserine, the addition of immunoglobulin E-directed ligands invariably led to an enhanced rate (approx. 4-fold) of labelling of phosphatidylinositol and, in the presence of Ca2+, this was accompanied by the secretion of histamine. The labelling of phosphatidylinositol and histamine secretion were also stimulated by chymotrypsin and compound 48/80. Whereas the phosphatidylinositol response did not require the presence of extracellular Ca2+, the secretion of histamine was either enhanced or dependent on extracellular Ca2+ (depending on the ligand used). The dependence on ligand concentration for the phosphatidylinositol response and histamine secretion were similar. The increased isotopic incorporation into phosphatidylinositol continued for about 1h although histamine secretion (elicited with concanavalin A) stopped within 2min. These results support the proposition that metabolic events involving phosphatidylinositol play a necessary intermediate role in the regulation of Ca2+ channels by ligand-activated receptors.


1994 ◽  
Vol 64 ◽  
pp. 92
Author(s):  
Mitsunobu Mio ◽  
Kiyomi Miyake ◽  
Masako Yamaji ◽  
Kenji Tasaka

1995 ◽  
Vol 10 (1) ◽  
pp. 75
Author(s):  
M. Aoki ◽  
M. Honda ◽  
O. Kawanami ◽  
G. Login ◽  
A. Dvorak

1988 ◽  
Vol 87 (2) ◽  
pp. 213-221 ◽  
Author(s):  
Kenji Tasaka ◽  
Masaaki Akagi ◽  
Kazuhisa Miyoshi ◽  
Mitsunobu Mio

2016 ◽  
Vol 310 (11) ◽  
pp. C894-C902 ◽  
Author(s):  
Amira Moustafa ◽  
Yoshiaki Habara

The aim of this study was to define the effects of polysulfide on intracellular Ca2+ concentration ([Ca2+]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 [Ca2+]i, which is both extracellular and intracellular Ca2+ dependent. Intracellular Ca2+ release induced by Na2S4 was attenuated by the addition of a ryanodine receptor blocker. A slow-releasing H2S donor, GYY4137, dose dependently increased [Ca2+]i that was independent from extracellular Ca2+ influx. The GYY4137-induced [Ca2+]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 [Ca2+]i elevation in the absence of extracellular Ca2+. An NO donor, diethylamine (DEA) NONOate, increased [Ca2+]i in a concentration-dependent manner, in which both extracellular and intracellular Ca2+ are associated. At higher concentrations, the DEA NONOate-induced [Ca2+]i increases were attenuated in the absence of extracellular Ca2+ 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 [Ca2+]i homeostasis in rat peritoneal mast cells via a cross talk with NO and H2S.


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