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The Effect of a Protein Kinase C Inhibitor, H‐7, on Human Neutrophil Oxidative Burst and Degranulation
Author(s) -
Berkow Roger L.,
Dodson Robert W.,
Kraft Andrew S.
Publication year - 1987
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.41.5.441
Subject(s) - degranulation , superoxide , protein kinase c , respiratory burst , nadph oxidase , chemotaxis , n formylmethionine leucyl phenylalanine , staurosporine , phorbol , granulocyte , biology , secretion , protein kinase inhibitor , superoxide dismutase , biochemistry , kinase , protein kinase a , microbiology and biotechnology , reactive oxygen species , enzyme , immunology , receptor
The role of C‐kinase in the activation of human polymorphonuclear leukocytes has been examined using H‐7, a recently described C‐kinase inhibitor. We found that H‐7 will inhibit PMN superoxide anion release in response to the tumor promotor phorbol myristate acetate and the calcium ionophore A23187. In contrast, no inhibition by H‐7 was seen for PMN superoxide release stimulated by the chemotactic peptide FMLP. H‐7 did not inhibit PMN NADPH oxidase activity or PMN degranulation by any stimulant, but it reversed a phorbol ester‐induced inhibition of granule release by FMLP. The results show that H‐7 differentially affects the PMN functional events of secretion and superoxide release and suggests that an H‐7 inhibitable C‐kinase 1) is not involved in chemotactic peptide induced activation of PMN and 2) may not regulate stimulus induced PMN degranulation.