Differentiation of second messenger systems in mast cell activation

Autor: White, J. R., Zembryki, D.
Zdroj: Inflammation Research; June 1989, Vol. 27 Issue: 3-4 p410-413, 4p
Abstrakt: Pretreatment of rat peritoneal mast cells with either Staurosporine or an analog K-252a, lead to a dose-related inhibition of histamine release when stimulated with Anti-IgE (IC50: Staurosporine=110 nM; K-252a=100 nM). In contrast, the two PKC inhibitors (1–1000 nM) failed to inhibit histamine release induced by compound 48/80 (0.5–1 μg/ml). Exposure of Anti-Asc-IgE sensitized mouse bone marrow derived mast cells to Asc-BSA lead to the release of both histamine (510 ng±12.6 ng/106 cells) and immunoreactive Leukotriene C4 (27.0±12.6 ng/106 cells) LTC4 release was inhibited by Staurosporine and K-252a with an IC50 of 75 nM for both compounds. Pretreatment of rat peritoneal mast cells with PMA 100 nM lead to a small but significant release of histamine (18.3±3.6%). Pretreatment of these cells with K-252a or Staurosporine lead to a dose related inhibition of histamine release with an ED50 of 10 nM for Staurosporine and 60 nM for K-252a. Treatment of rat peritoneal mast cells with the calcium ionophore A23187 lead to a significant release of histamine which was not inhibited by either of the two kinase inhibitors (0.1–1000 nM). The two kinase inhibitors also inhibited mouse bone marrow derived mast cell proliferation in response to IL-3 with IC50 of 80 nM for Staurosporine and 270 nM for K-252a.
Databáze: Supplemental Index