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Mast cell activation by pedicellarial toxin of sea urchin, Toxopneustes pileolus
Author(s) -
Takei Masao,
Nakagawa Hideyuki,
Endo Koichi
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80965-w
Subject(s) - pertussis toxin , cholera toxin , histamine , toxin , mast cell , clostridium difficile toxin a , sea urchin , phospholipase c , anthrax toxin , inositol trisphosphate , marine toxin , biology , inositol , chemistry , biochemistry , microbiology and biotechnology , g protein , pharmacology , endocrinology , receptor , immunology , recombinant dna , clostridium difficile , gene , fusion protein , antibiotics
Pedicellarial toxin, partially purified from the sea urchin Toxopneustes pileolus , dose‐dependently and time‐dependently caused histamine release from rat peritoneal mast cells. Pedicellarial toxin induced a rapid initial rise in [Ca 2+ ] i within several seconds which was followed by a further slower increase of [Ca 2+ ] (second rise). The toxin induced a dose‐dependent formation of inositol 1,4,5‐triphosphate (IP3) as well as the histamine release in mast cells. Furthermore, the toxin stimulated phosphoinositide‐specific phospholipase C (PI‐PLC) activity in mast cell membranes. 2‐Nitro‐4‐carboxyphenyl‐ N , N . ‐diphenylcarbamate (NCDC), a PLC inhibitor, inhibited the activation of PI‐PCL induced by pedicellarial toxin. Cholera toxin inhibited pedicellarial toxin‐induced histamine release, whereas pretreatment of pertussis toxin failed to inhibit it. These results suggest that pedicellarial toxin from T. pileolus activates PI‐PCL and the stimulation of PI turnover may lead to the release of IP3 into the cytoplasm, resulting in histamine release from rat mast cells.