Abstract
IP3, a product of phospholipase C-induced phosphoinositide hydrolysis has been proposed as an intracellular messenger generated by receptor stimulation of cells. I?3 has been shown to cause Ca++ release from intracellular stores in permeabilized pancreatic acinar cells and hepatocytes. The effect of IP3 on platelet aggregation and ultrastructure was studied using washed human platelets permeabilized with saponin and suspended in a Ca++-free buffer (120 mM KC1, 4.9 mM NaCl, 1.2 mM KH2PO4, 1.2 mM MgCl2, 10 mM HEPES, 15 mM dextrose, 0.2% albumin, pH 7.4). Aggregation occurred with an IP3 concentration of 0.5 μM, with maximum aggregation obtained at 10 μM. No aggregation occurred either with saponin alone or with IP3 in non-permeabilized platelets. Examination of ultrastructure revealed aggregates with centralization of granules, typical of morphologic changes seen with increases in cytoplasmic Ca++. These findings suggest that IP3 produced during platelet stimulation may act as a second messenger to promote Ca++ flux and may serve a similar function in other cells.
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Israels, S., Gerrard, J. 916 AGGREGATION OF PERMEABILIZED PLATELETS IN RESPONSE TO INOSITOL TRIPHOSPHATE (IP3). Pediatr Res 19, 263 (1985). https://doi.org/10.1203/00006450-198504000-00946
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DOI: https://doi.org/10.1203/00006450-198504000-00946