Metabolic aspects of the secretion of stored compounds from blood platelets. The effect of NaF at different pH on nucleotide metabolism and function of washed platelets

Mürer, Erik H.; Davenport, Katherine P.; Siojo, E; Day, H. James

doi:10.1042/bj1940187

Cited by 16 publications

(5 citation statements)

References 17 publications

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“…However, the potentiation by AlCl3 was more evident when NaF had been preincubated for 5 min with platelets. This agrees with an early report on NaF-induced aggregation and release, which were shown to occur after a lag of at least 6 min (Miirer, 1968), the time required for NaF to penetrate the cell (Murer et al, 1981).…”

Section: Aggregation and Releasesupporting

confidence: 93%

How does fluoroaluminate activate human platelets?

Rendu

Lebret

Tenza

et al. 1990

Biochemical Journal

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Platelet activation induced by NaF or fluoroaluminate (AlF4-) was studied. The latter has been described to substitute for the gamma-phosphate group of the GTP molecule. With 10 mM-NaF, a concentration unable to induce any measurable Ca2+ mobilization (as measured with Indo 1), addition of AlCl3 potentiated platelet aggregation, thromboxane synthesis, diacylglycerol formation and p43 phosphorylation, without any increase in intracellular Ca2+. Neither phosphoinositide hydrolysis nor phosphatidic acid formation could be detected. AlF4- induced the release through a granule centralization within a microtubule bundle, although no myosin light-chain phosphorylation could be detected. Addition of flurbiprofen (10 microM) resulted in only partial inhibition of diacylglycerol formation, with no effect on the release reaction or on p43 phosphorylation. The present results suggest that AlF4- does not stimulate a G-protein governing the phosphoinositide-specific phospholipase C. The AlF4(-)-induced diacylglycerol formation is discussed. Moreover, these results bring evidence that there is no correlation between granule centralization and myosin light-chain phosphorylation.

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Section: Aggregation and Releasesupporting

confidence: 93%

How does fluoroaluminate activate human platelets?

Rendu

Lebret

Tenza

et al. 1990

Biochemical Journal

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“…Fluoride also increased intracellular cal cium levels in human platelets (41) and neutrophils (40) . The ability of fluor ide to stimulate the formation of Insl ,4,5P3 and to elevate calcium levels in intact cells may explain how this ion can stimulate the release reaction of platelets (42), and can mimic the effect of light in Limulus photoreceptors (43).…”

Section: Hydrolysis Of Ptdins45p2mentioning

confidence: 99%

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Berridge¹

1987

Annu. Rev. Biochem.

3,261

1,335

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“…Deamination of AMP may also serve in the stabilization of the AEC, as has been shown for several tissues (Chapman et al, 1976;Atkinson, 1977;Matsumoto et al, 1979;Pradet & Raymond, 1983). AEC values around 0.9 appear crucial for normal platelet function (Holmsen & Robkin, 1977;Murer et al, 1981;Akkerman et al, 1983). Whereas aggregation and secretion responses remain unaffected by H202 treatment (Holmsen & Robkin, 1977;Verhoeven et al, 1985), starvation leads to a gradual loss in platelet function in parallel with a lowering of AEC (Akkerman et al, 1983).…”

Section: Discussionmentioning

confidence: 92%

“…Previously, H202 has been shown to induce a quantitative shift of phosphate from cytosolic ATP to glycolytic intermediates, notably fructose 1,6-bisphosphate and dihydroxyacetone phos-phate (Verhoeven et al, 1985). Depletion of the cytosolic adenylate pool through deamination of AMP was also observed upon treatment of platelets with plateletactivating agents (Akkerman et al, 1984), cyanide (Akkerman et al, 1984), fluoride (Murer et al, 1981) and low doses of 2-deoxyglucose (Holmsen et al, 1974;Holmsen & Robkin, 1980). In all of these conditions, ATP catabolism is accompanied by an unaltered or decreased rather than increased intracellular P1 concentration.…”

Section: Discussionmentioning

confidence: 94%

“…In platelets, the AMP dephosphorylation route appears to be absent (Harris & Crawford, 1973;Holmsen et al, 1974). Upon platelet activation (Holmsen et al, 1972;Fukami et al, 1976) or when platelets are exposed to metabolic stress (Holmsen & Robkin, 1977Murer et al, 1981;Holmsen, 1985), AMP deaminase is stimulated so that hardly any AMP accumulates, and the decrease in cytosolic ATP and ADP is almost completely recovered in IMP and its degradation products, inosine and hypoxanthine. As a result the adenylate energy charge (AEC), defined as follows: AEC = (ATP + 'ADP)/(ATP + ADP + AMP) (Atkinson, 1977), is maintained at a high value.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of platelet AMP deaminase activity in situ

Verhoeven

Marszałek

Holmsen

1990

Biochemical Journal

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The regulation of platelet AMP deaminase activity by ATP, GTP and phosphate was studied in human platelets in situ, and in vitro after partial purification. In intact platelets, a similar 50% decrease in cytosolic ATP was induced by either glucose starvation or treatment with H2O2. During starvation, AMP deaminase was in the inhibited state, as ATP consumption was mostly balanced by the accumulation of AMP. During H2O2 treatment, however, the enzyme was in the stimulated state, as the AMP formed was almost completely deaminated to IMP. Cytosolic GTP fell by 40-50% in both starvation and H2O2 treatment. In contrast, intracellular phosphate was 4-5-fold higher in starved than in H2O2-treated cells. These data point to phosphate as the main regulator of AMP deaminase activity in situ. This conclusion was verified by kinetic analysis of partially purified AMP deaminase. At near-physiological concentrations of MgATP, MgGTP and phosphate, the S0.5 (substrate half-saturation constant) for AMP was 0.35 mM. Half-maximal stimulation by MgATP occurred at a concn. between 2 and 3 mM. This stimulation was antagonized by the inhibitory effects of phosphate (IC50 = 2.0 mM) and MgGTP (IC50 = 0.2-0.3 mM), which acted in synergism (IC50 is the concentration causing 50% inhibition). We conclude that the difference in adenylate catabolism between starved and H2O2-treated platelets is due to the distinct phosphate concentrations. During starvation, refeeding and H2O2 treatment, the values of the adenylate charge and the phosphorylation potential were kept closely co-ordinated, which may be effected by AMP deaminase.

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Metabolic aspects of the secretion of stored compounds from blood platelets. The effect of NaF at different pH on nucleotide metabolism and function of washed platelets

Abstract: The purpose of this study was to investigate the response of human blood platelets to fluoride at different pH. The results were as follows. (1)

Cited by 16 publications

References 17 publications

How does fluoroaluminate activate human platelets?

How does fluoroaluminate activate human platelets?

Inositol Trisphosphate and Diacylglycerol: Two Interacting Second Messengers

Regulation of platelet AMP deaminase activity in situ

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