Literature DB >> 2177621

Positive feedback regulation of phospholipase C by vasopressin-induced calcium mobilization in WRK1 cells.

B Mouillac1, M N Balestre, G Guillon.   

Abstract

In WRK1 cells vasopressin stimulates Ins(1,4,5)P3 accumulation and mobilizes intracellular calcium. These two phenomena are transient and exhibit similar time-courses. Experiments performed on intact cells or membrane preparations demonstrate that calcium may also stimulate an accumulation of inositol phosphates. This suggests a possible positive feedback regulation of the primary accumulation of Ins(1,4,5)P3 induced by vasopressin. In order to test such a possibility we studied the vasopressin-induced Ins(1,4,5)P3 accumulation, where intracellular calcium mobilization is artificially suppressed by incubating the cells with EGTA in the presence of ionomycin. Under these conditions the accumulation of Ins(1,4,5)P3 induced by 1 microM vasopressin is inhibited by around 50% when measured 5 s after stimulation. This inhibition is not due to an alteration of the VIa vasopressin receptor binding properties, a reduction of the amount of substrate available for the phospholipase C, a stimulation of the Ins(1,4,5)P3 5-phosphatase or an activation of the Ins(1,4,5,)P3 kinase. It is more likely the consequence of the suppression of calcium wave generated by Ins(1,4,5)P3 which may in its turn stimulate a phospholipase C. Different arguments favour this hypothesis: (1) calcium at an intracellular physiological concentration (0.1-1 microM) is able to stimulate a phospholipase C; (2) artificially increasing the [Ca2+]i inside the WRK1 cell induces an accumulation of Ins(1,4,5)P3; and (3) the time-course of the inhibition of Ins(1,4,5)P3 accumulation induced by an EGTA/ionomycin treatment correlates well with that of the calcium mobilization. Altogether these results suggest that Ins(1,4,5)P3 accumulation in WRK1 cells may result from two distinct mechanisms: a direct vasopressin receptor-mediated PLC activation which is independent of calcium and a calcium-mediated PLC activation related to the intracellular calcium mobilization.

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Year:  1990        PMID: 2177621     DOI: 10.1016/0898-6568(90)90046-d

Source DB:  PubMed          Journal:  Cell Signal        ISSN: 0898-6568            Impact factor:   4.315


  7 in total

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Journal:  J Comput Neurosci       Date:  2012-03-28       Impact factor: 1.621

3.  Close association of the alpha subunits of Gq and G11 G proteins with actin filaments in WRK1 cells: relation to G protein-mediated phospholipase C activation.

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4.  Release of Ca2+ is the crucial step for the potentiation of IPSCs in the cultured cerebellar Purkinje cells of the rat.

Authors:  T Hashimoto; T Ishii; H Ohmori
Journal:  J Physiol       Date:  1996-12-15       Impact factor: 5.182

5.  Extracellular calcium concentration controls the frequency of intracellular calcium spiking independently of inositol 1,4,5-trisphosphate production in HeLa cells.

Authors:  M D Bootman; K W Young; J M Young; R B Moreton; M J Berridge
Journal:  Biochem J       Date:  1996-02-15       Impact factor: 3.857

6.  Two roles of Ca2+ in agonist stimulated Ca2+ oscillations.

Authors:  J Keizer; G W De Young
Journal:  Biophys J       Date:  1992-03       Impact factor: 4.033

7.  An age-dependent feedback control model of calcium dynamics in yeast cells.

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Journal:  J Math Biol       Date:  2009-08-12       Impact factor: 2.259

  7 in total

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