Am J Physiol Cell Physiol Journal of Applied Physiology
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Am J Physiol Cell Physiol 280: C789-C795, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 4, C789-C795, April 2001

PLD pathway involved in carbachol-induced Clminus secretion: possible role of TNF-alpha

Judith C. J. Oprins, Claudia van der Burg, Helen P. Meijer, Teun Munnik, and Jack A. Groot

Swammerdam Institute for Life Sciences, University of Amsterdam, 1090 GB Amsterdam, The Netherlands

In a previous study, it was found that exposure to tumor necrosis factor-alpha (TNF-alpha ) potentiated the electrophysiological response to carbachol in a time-dependent and cycloheximide-sensitive manner. It was deduced that the potentiation could be due to protein kinase C activity because of increased 1,2-diacylglycerol. It was also observed that propranolol could decrease the electrophysiological response to carbachol (Oprins JC, Meijer HP, and Groot JA. Am J Physiol Cell Physiol 278: C463-C472, 2000). The aim of the present study was to investigate whether the phospholipase D (PLD) pathway plays a role in the carbachol response and the potentiating effect of TNF-alpha . The transphosphatidylation reaction in the presence of the primary alcohol 1-butanol [leading to stable phosphatidylbutanol (Pbut) formation] was used to measure activity of PLD. The phosphatidic acid (PA) levels were also measured. Muscarinic stimulation resulted in an increased formation of Pbut and PA. TNF-alpha decreased levels of PA.

intestinal epithelia; protein kinase C; phosphatidic acid; thin-layer chromatography


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