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Research Article Free access | 10.1172/JCI115594

Long-term activation of protein kinase c causes chronic Na/H antiporter stimulation in cultured proximal tubule cells.

S Horie, O Moe, R T Miller, and R J Alpern

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Horie, S. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Moe, O. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Miller, R. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Alpern, R. in: JCI | PubMed | Google Scholar

Published February 1, 1992 - More info

Published in Volume 89, Issue 2 on February 1, 1992
J Clin Invest. 1992;89(2):365–372. https://doi.org/10.1172/JCI115594.
© 1992 The American Society for Clinical Investigation
Published February 1, 1992 - Version history
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Abstract

To examine the role of protein kinase C as a chronic regulator of proximal tubule Na/H antiporter activity, the effect of phorbol 12-myristate 13-acetate (PMA) on the Na/H antiporter was studied in cultured proximal tubule cells. Short-term activation of protein kinase C by 5 min exposure to PMA caused an acute increase in Na/H antiporter activity that was not prevented by cycloheximide or actinomycin D and did not persist 24 h later. Long-term activation of protein kinase C by 2 h exposure to PMA caused a dose-dependent increase in Na/H antiporter activity 24 h later. This latter effect was due to protein kinase C activation in that it was inhibited by sphingosine and was not seen with 4 alpha-PMA, an inactive analogue. The chronic effect of PMA was inhibited by 10 nM actinomycin D or 7 microM cycloheximide. Proximal tubule cells exposed to PMA for 2 h demonstrated a two- to threefold increase in Na/H antiporter mRNA (mRNANa/H) abundance 4 h later. In conclusion, short-term activation of protein kinase C leads to a transient increase in Na/H antiporter activity that is independent of transcription and translation, whereas long-term activation of protein kinase C causes a persistent increase in antiporter activity that is dependent on transcription and translation and is associated with increased mRNANa/H abundance. This latter effect may mediate increased Na/H antiporter activity in a number of chronic conditions.

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