Regulation of p-aminohippurate transport by protein kinase c in ok
kidney epithelial cells.
Takano, Mikihisa, Junya Nagai, Masato Yasuhara, and Ken-Ichi Inui.
Department of Pharmacy, Kyoto University Hospital, Faculty of
Medicine, Kyoto University, Sakyo-ku, Kyoto 606-01, Japan
APStracts 3:0089F, 1996.
We studied the effect of phorbol 12-myristate 13-acetate (PMA), a
phorbol ester which activates protein kinase C, on p-aminohippurate
(PAH) transport in OK cells. PMA (10-7 M) almost completely inhibited
the transcellular transport of PAH across OK cell monolayers from the
basal to the apical side, as well as the accumulation of PAH in the
cells. The uptake of PAH across the basolateral membrane of OK cells
was inhibited by PMA in a time- and dose-dependent fashion. Exposing
the cells with other protein kinase C activators such as active
phorbol esters and diacylglycerols also resulted in a significant
inhibition of basolateral PAH uptake, but the inactive phorbol ester,
4[alpha]-phorbol 12,13-didecanoate, had no effect. The inhibition of
basolateral PAH uptake by PMA was blocked by staurosporine, an
inhibitor of protein kinase C. Cycloheximide, actinomycin D,
colchicine and cytochalasin D did not affect the inhibitory effect of
PMA on basolateral PAH uptake. These results suggested that the PAH
transport system in OK cells is under the regulatory control of
protein kinase C.
Received 27 November 1995; accepted in final form 25 April 1996.
APS Manuscript Number F398-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 May 96