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Elevation of Intracellular Calcium Ion by Prostaglandin E1 and Its Inhibition by Protein Kinase C in a Human Megakaryocyte Leukemia Cell Line

Elevation of Intracellular Calcium Ion by Prostaglandin E1 and Its Inhibition by Protein Kinase C in a Human Megakaryocyte Leukemia Cell Line

M Adachi, R Ryo, A Yoshida, K Teshigawara, N Yamaguchi, M Hoshijima, Y Takai, T Sato

Cancer Res. 1989 Jul 15;49(14):3805-8.

PMID: 2736522

Abstract:

In the present study, we examined the effect of prostaglandin E1 (PGE1) on Ca2+ mobilization in a human megakaryocyte (the progenitor of platelets) leukemia cell line, designated as CMK. PGE1 caused a rapid and dose-dependent increase in the intracellular free calcium level ([Ca2+]i) associated with the elevation of cyclic AMP. The PGE1-induced elevation of [Ca2+]i was decreased by the prior addition of ethylene glycol bis(2-aminoethylether)tetraacetic acid to the medium by approximately 25% of the control. This result indicates that the PGE1-induced elevation of [Ca2+]i is due to influx of Ca2+ from the external medium and to mobilization of Ca2+ from intracellular stores. Pretreatment of CMK cells with 12-O-tetradecanoylphorbol-13-acetate (TPA), a stimulus for protein kinase C, further enhanced the PGE1-induced increase in the cellular cyclic AMP level. Inversely, pretreatment of CMK cells with TPA (10 nM), prior to the addition of PGE1, inhibited the PGE1-induced elevation of [Ca2+]i. Dibutyryl cyclic AMP and forskolin did not elevate [Ca2+]i or affect the PGE1-induced Ca2+ mobilization. The inhibitory action of TPA in the PGE1-induced elevation of [Ca2+]i was mimicked by other protein kinase C-activating agents, such as 1-oleoyl-2-acetylglycerol and N-(6-phenylhexyl)-5-chloro-1-naphthalenesulfonamide, and was selectively restored by protein kinase C inhibitors, such as 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride and N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride. Thus, the inhibitory modulation of TPA on the PGE1-induced elevation of [Ca2+]i is mediated through protein kinase C activation. PGE1 had no inductional effect of megakaryocytic phenotypic changes in CMK cells. The biological role of PGE1, which increased [Ca2+]i and cyclic AMP levels in the CMK cells, remains to be determined.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP102649785	N-(6-Phenylhexyl)-5-chloro-1-naphthalenesulfonamide		102649-78-5	Price

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