Involvement of Protein Kinase C in Prostaglandin E 2-induced Catecholamine Release from Cultured Bovine Adrenal Chromaffin Cells

Content Provider	Semantic Scholar
Author	Negishi, Manabu Ito, Seiji Osamu Hayaishi S.
Copyright Year	2001
Abstract	We recently reported that prostaglandin (PG) Ez stimulated phosphoinositide metabolism in cultured bovine adrenal chromaffin cells and that PGEz and ouabain induced a gradual secretion of catecholamines from the cells (Yokohama, H., Tanaka, T., Ito, S., Negishi, M., Hayashi, H., and Hayaishi, 0. (1988) J. Biol. Chem. 263, 1119-l 122). Here we examined the involvement of two signal pathways, Ca2+ mobilization and protein kinase C activation resulting from phosphoinositide metabolism, in the PGEz-induced catecholamine release. Either the Ca2+ ionophore ionomytin or 12-0-tetradecanoylphorbol 13-acetate (TPA) could enhance the release in the presence of ouabain, and ionomycin-induced release was additive to PGE2induced release, but TPA-induced release was not additive. PGEz dose-dependently stimulated the formation of diacylglycerol and caused the translocation of 4% of the total protein kinase C activity to become membrane-bound within 5 min. These effects were specific for PGEz and PGE, among PGs tested (PGE2 = PGEl > PGF2, > PGD2). Furthermore, the phosphoinositide-specific phospholipase C inhibitor neomycin inhibited PGEz-induced accumulation of inositol phosphates, diacylglycerol formation, translocation of protein kinase C, and also stimulation of catecholamine release. Both PGE2and TPA-induced release were inhibited by the depletion of protein kinase C caused by prolonged exposure to TPA, but ionomycin-induced release was not inhibited. We recently found that the amiloride-sensitive Na+, H+-antiport participates in PGEz-evoked catecholamine release (Tanaka, T., Yokohama, H., Negishi, M., Hayashi, H., Ito, S., and Hayaishi, 0. (1990) J. Neurochem. 54, 86-95). In agreement with our recent report, PGEz and TPA induced a sustained increase in intracellular pH that was abolished by the protein kinase C inhibitor staurosporine but not by the calmodulin inhibitor W-7. Ionomycin also induced a marked increase in intracellular pH, but this increase was abolished by W-7 but not by staurosporine. These results demonstrate that PGEz-induced activation of the Na+, H+-antiport and catecholamine release in the presence of ouabain are mediated by activation of protein kinase C, rather than by Ca2+
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Language	English
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Content Type	Text
Resource Type	Article