Protein kinase C has both stimulatory and suppressive effects on macrophage superoxide production

Abstract

Unlike resident peritoneal macrophages (RPM) or tumor necrosis factor α (TNFα)‐primed bone marrow‐derived macrophages (BMM), unprimed BMM do not generate superoxide in response to the protein kinase C (PKC) activator, phorbol myristate acetate (PMA). However, these cells do contain significant levels of PKC activity. In contrast to PMA, zymosan induces the generation of superoxide in unprimed BMM, as well as in TNFα‐primed BMM and RPM. Staurosporine, a potent PKC inhibitor, failed to affect the zymosan‐induced production of superoxide by unprimed and TNFα‐primed BMM and RPM, in spite of substantial inhibition of PMA‐induced superoxide production by the primed BMM and RPM. However, when PKC w..