PMID: 2508487Oct 1, 1989Paper

Mechanism of phorbol ester inhibition of histamine-induced IP3 formation in cultured airway smooth muscle

The American Journal of Physiology
R K MurrayM I Kotlikoff

Abstract

Cytosolic calcium is a key determinant of the contractile state of airway smooth muscle (ASM). To investigate the mechanisms by which histamine affects cytosolic calcium, we measured changes in inositol 1,4,5-trisphosphate (IP3) following the addition of histamine to cultured canine ASM cells. The effect of phorbol 12-myristate 13-acetate (PMA) on IP3 formation was investigated under conditions previously shown to abolish histamine-induced calcium release. In both intact cells and ASM membranes, histamine produced a significant increase in IP3 formation, which was inhibited by PMA. The site of this blockade was investigated by examining the effect of PMA on guanine nucleotide-stimulated IP3 formation and on phosphoinositide-specific phospholipase C (PI-PLC) activity in ASM membranes. Guanine nucleotide-stimulated IP3 formation was inhibited by PMA pretreatment. Membrane-associated PI-PLC activity was also decreased, an effect that was not due simply to a shift in the calcium sensitivity of the enzyme. We conclude that in cultured canine ASM cells, PMA blocks histamine-induced IP3 formation and that this inhibition is caused, in part, by a postreceptor site of action of protein kinase C, possibly via a direct effect on PI-PLC.

Citations

Apr 12, 2005·American Journal of Physiology. Lung Cellular and Molecular Physiology·Deepak A DeshpandeMathur S Kannan
Apr 6, 2001·American Journal of Physiology. Lung Cellular and Molecular Physiology·S A Barman

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