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  • Title: Involvement of calcium in phosphoinositide metabolism in the blood-brain barrier.
    Author: Catalán RE, Martínez AM, Aragonés MD, Fernández I, Hernández F.
    Journal: Cell Signal; 1995 Mar; 7(3):261-7. PubMed ID: 7662512.
    Abstract:
    The Ca2+ effect on phosphoinositide metabolism in the blood-brain barrier was studied by using rat cerebral microvessels prelabelled with either [32P]orthophosphate or myo-[3H]inositol and stimulated with Ca2+ ionophore A23187. In radioactivity steady-state conditions, addition of ionophore caused a rapid and marked loss of labelling in both phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2), without significant alterations in phosphatidylinositol (PI) and phosphatidic acid (PA) labelling. These facts were accompanied by a rise in labelling of both inositol 1-monophosphate (IP) and inositol 1,4-bisphosphate (IP2), but not in inositol 1,4,5-trisphosphate (IP3). In addition, a Ca(2+)-dependent inhibition of phosphoinositide kinase activities from isolated membranes was also found. These data suggest that elevated intracellular Ca2+ level evokes a PIP and PIP2 hydrolysis by phosphodiesterasic and phosphomonoesterasic activities respectively, and also partially inhibits the synthesis of these phosphoinositides. Our results constitute evidence that a reciprocal control mechanism between polyphosphoinositide metabolism and mobilization of Ca2+ exists in the blood-brain barrier.
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