Abstract
Bone marrow-derived mouse mast cells were sensitized with monoclonal mouse IgE antibody and treated with cholera toxin (CT), which ADP-ribosylated the α-subunit of the stimulatory guanine nucleotide-binding regulatory protein G(s), prior to challenge with either antigen or thrombin. The CT treatment inceased intracellular cAMP levels, but neither enhanced nor inhibited antigen-induced histamine release or arachidonate release. The same treatment of the sensitized bone marrow-derived mouse mast cells with CT markedly enhanced thrombin-induced histamine release without affecting arachidonate release. The CT treatment failed to affect antigen-induced and thrombin-induced generation of inositol triphosphate and of diacylglycerol or mobilization of intracellular Ca2+. The results indicate that G(s) in bone marrow-derived mouse mast cells is not involved involved in the transduction of the antigen-induced or thrombin-induced triggering signal to phospholipase C, which initiates the enhancement of phosphatidylinositol turnover. The enhancement of thrombin-induced histamine release by CT treatment with the observations that thrombin-induced histamine release was inhibited by pretreatment of the cells with pertussis toxin suggest that the involvement of a guanine nucleotide-binding regulatory protein in thrombin-induced biochemical events is an event distal to Ca2+ mobilization.
Original language | English (US) |
---|---|
Pages (from-to) | 2504-2508 |
Number of pages | 5 |
Journal | Proceedings of the National Academy of Sciences of the United States of America |
Volume | 85 |
Issue number | 8 |
DOIs | |
State | Published - 1988 |
Externally published | Yes |
ASJC Scopus subject areas
- General