Kinoshita Y, Fukase M, Hishikawa R, Fujita T
Department of Medicine, Kobe University School of Medicine, Japan.
Endocrinol Jpn. 1988 Apr;35(2):217-23. doi: 10.1507/endocrj1954.35.217.
To assess the role of protein kinase C and cAMP on the calcitonin-induced alteration of phosphate accumulation by renal tubular cells, the effects of phorbol esters, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and DBcAMP on the phosphate accumulation in LLC-PK1 cells were investigated. Calcitonin stimulated phosphate accumulation with a concomitant increase in cAMP production. Phorbol esters and 1-oleoyl-2-acetyl-glycerol, activators of protein kinase C, also stimulated the phosphate accumulation. Furthermore, H-7, an inhibitor of protein kinase C, inhibited a calcitonin-induced increase in phosphate accumulation significantly. Although DBcAMP by itself did not increase the phosphate accumulation, it enhanced the stimulatory effect of 12-0-tetradecanoyl phorbol-13-acetate on the phosphate accumulation. Accordingly, protein kinase C as well as cAMP might be involved in the calcitonin-induced increase in phosphate accumulation in LLC-PK1 cells.
