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  • Title: Does protein kinase C regulate receptor agonists-mediated elevation in the cytosolic Ca2+ in human neutrophils?
    Author: Tuominen H, Leino L, Akerman KE.
    Journal: Biochem Biophys Res Commun; 1994 Sep 15; 203(2):998-1004. PubMed ID: 8093086.
    Abstract:
    The feedback regulation of elevated cytosolic free Ca2+ concentrations ([Ca2+]i) by protein kinase C (PKC) in neutrophils was studied by two approaches. First, the PKC-activity was induced by phorbol 12-myristate 13-acetate (PMA) before the stimulation of Ca2+-signal with N-formyl-methionyl-leucyl-phenylalanine and serum-opsonized zymosan particles. Pretreatment of cells with PMA inhibited agonists-dependent Ca(2+)-transients. This inhibition was reversed by staurosporine. Second, the PKC-activity was induced simultaneously with the Ca(2+)-signal by the receptor agonists. In these conditions staurosporine had no effect on the Ca(2+)-response. In addition, the enhancement of PKC-activity, obtained by accumulating the endogenous PKC-activator diacylglycerol (DAG) with a DAG-kinase inhibitor, failed to change the agonists-stimulated elevations of [Ca2+]i. It is concluded that activation of PKC by PMA inhibits neutrophil Ca(2+)-responses, whereas receptor-mediated activation of PKC does not yield a negative feedback in elevated [Ca2+]i.
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