Abstract
Interleukin 3-dependent BNu-2c13 mast cells, mucosal type-like mast cells, exhibited a specific high-affinity binding site for [ 3H]prostaglandin (PG) E 2. The binding was completely displaced by M&B 28767, an EP 3-selective agonist, but not by EP 1- or EP 2-selective ligands, indicating that the PGE 2 binding site is of the EP 3 subtype PGE receptor. Whereas the EP 3 subtype is presumed to be coupled to inhibition of adenylate cyclase in various tissues and cells, in BNu-2c13 cells PGE 2 had no ability to inhibit adenylate cyclase activity, while it induced concentration-dependent stimulation of phosphoinositide metabolism and caused an increase in the intracellular free Ca 2+ concentration in a pertussis toxin-sensitive manner. PGE 2 by itself did not evoke histamine release from the cells, but it markedly stimulated histamine release in concert with ionomycin, a Ca 2+ ionophore. The PGE 2-stimulated release was also comletely blocked by pertussis toxin. Thus, the PGE receptor expressed on BNu-2c13 mast cells is of the EP 3 subtype and is linked to phosphoinositide metabolism via a pertussis toxin-sensitive G protein, and this activation leads to histamine release.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
