Hydrolysis of cell surface phosphatidylinositol leads to the delayed stimulation of inositol phospholipid synthesis in Bovine Aortic Endothelial Cells

Date

1993

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Article

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Yes

Abstract

In order to address the issue of how inositol phospholipid synthesis is controlled in a resting cell we looked for enhanced [3H]phosphatidylinositol (PtdIns) labelling in response to the hydrolysis of cell surface PtdIns. Bacillus thuringiensis PtdIns-PLC when added to intact bovine aortic endothelial (BAE) cells rapidly hydrolysed 9.1 +/- 1% of the total cellular PtdIns. This result suggests that BAE cells have a cell surface pool of PTdIns. Hydrolysis of cell surface PtdIns, in contrast to the agonist-stimulated hydrolysis of inner leaflet PtdIns, did not lead to a rapid (minutes) stimulation of PtdIns resynthesis. Prolonged incubation of BAE cells with PtdIns-PLC led to further hydrolysis of PtdIns (up to 20% of total cellular PtdIns). This second phase of PtdIns-PLC induced hydrolysis was inhibited by the addition of brefeldin A suggesting that it was dependent on vesicular traffic to the plasma membrane from the endoplasmic reticulum. Furthermore, the above result suggests that prolonged incubation of intact cells with PtdIns-PLC leads to the slow depeletion of intracellular PtdIns stores. This second phase of PtdIns-PLC induced hydrolysis was associated with PtdIns resynthesis since prolonged incubation with PtdIns-PLC, but not B. cereus PtdCho-PLC (which does not hydrolyse PtdIns), led to enhanced PtdIns labelling. The results indicate that extracellular PtdIns-PLC induced PtdIns resynthesis may occur due to PtdIns-PLC induced intracellular PtdIns depletion.

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Sillence, D.J. and Low, M.G. (1993) Hydrolysis of cell surface phosphatidylinositol leads to the delayed stimulation of inositol phospholipid synthesis in Bovine Aortic Endothelial Cells. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1224 (2), pp. 247-254

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Leicester Institute for Pharmaceutical Innovation - From Molecules to Practice (LIPI)