Rapid decrease of phosphatidylinositol 4,5-bisphosphate in thrombin-stimulated platelets.

Billah, M. Motasim; Lapetina, Eduardo G.

doi:10.1016/s0021-9258(18)33568-3

Cited by 312 publications

(8 citation statements)

References 38 publications

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“…The ether-linked lipid 1-O-alkyl, 2-acetyl, phosphorylcholine is a highly potent platelet-activating factor, in part responsible for stimulating the secretion of platelet-derived growth factor for use in wound healing (for review see reference 2). In other secretory systems there is also evidence for the involvement of lipid factors (3,6,8,14,19,21,29). Phosphokinase-C (24) requires the presence of specific diacylglycerol molecules (synthesized by phosphatidyl inositol breakdown) for its enzymatic activity, perhaps acting to bring the kinase to the membrane from its normal location in the cytoplasm.…”

Section: Relationship Of These Experiments To the Mechanisms Of Cell Fusionmentioning

confidence: 99%

Biochemical studies on cell fusion. II. Control of fusion response by lipid alteration.

Roos¹,

Choppin²

1985

The Journal of Cell Biology

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The preceding communication (Roos, D. S. and P. W. Choppin, 1985, J. Cell Biol. 101:1578-1590 described the lipid composition of a series of mouse fibroblast cell lines which vary in susceptibility to the fusogenic effects of polyethylene glycol (PEG). Two alterations in lipid content were found to be directly correlated with resistance to PEG-induced cell fusion: increases in fatty acyl chain saturation, and the elevation of neutral glycerides, including an unusual ether-linked compound. In this study, we have probed the association between lipid composition and cell fusion through the use of fatty acid supplements to the cellular growth medium, and show that the fusibility of cells can be controlled by altering their acyl chain composition. The parental Clone 1D cells contain moderately unsaturated fatty acids with a ratio of saturates to polyunsaturates (S/P) ,~ 1, and fuse virtually to completion following a standard PEG treatment. By contrast, the lipids of a highly fusion-resistant mutant cell line, F40, are highly saturated (S/P = 4). When the S/P ratio of Clone 1D cells was increased to approximate that normally found in F40 cells by growth in the presence of high concentrations of saturated fatty acids, they became highly resistant to PEG. Reduction of the S/P ratio of F40 cells by growth in cis-polyunsaturated fatty acids rendered them susceptible to fusion. Cell lines Fa, F16, etc., which are normally intermediate between Clone 1D and F40 in both lipid composition and fusion response, can be altered in either direction (towards either increased or decreased susceptibility to fusion) by the addition of appropriate fatty acids to the growth medium. Although trans-unsaturated fatty acids have phase-transition temperatures roughly similar to saturated compounds, and might therefore be expected to affect membrane fluidity in a similar manner, trans-unsaturated fatty acids exerted the same effect as cisunsaturates on the control of PEG-induced cell fusion. This observation suggests that the control of cell fusion by alteration of fatty acid content is not due to changes in membrane fluidity, and thus that the fatty acids are involved in some other way in the modulation of cell fusion.

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Section: Relationship Of These Experiments To the Mechanisms Of Cell Fusionmentioning

confidence: 99%

Biochemical studies on cell fusion. II. Control of fusion response by lipid alteration.

Roos¹,

Choppin²

1985

The Journal of Cell Biology

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“…Activation of platelets involves the production of stimulatory second messengers such as IP3 and diacylglycerol and a rise in cytosolic Ca2+ concentrations (Billah and Lapetina, 1982;Berridge, 1984;Nishizuka, 1984;Watson et al, 1985). Results presented here demonstrate that Cvx causes the aggregation of platelets and PLC activation to an extent similar to those with high concentrations of thrombin.…”

Section: Discussionmentioning

confidence: 57%

“…Our results show that aggregation and the breakdown of inositol phospholipids in washed rabbit platelets induced by a high concentration of Cvx is only partially inhibited by neomycin, an aminoglycoside antibiotic which inhibits PLC activity. Under similar conditions, neomycin suppresses the effects of thrombin and U46619, two powerful stimulators of platelet aggregation and of PLC activation (Billah and Lapetina, 1982;Siess et al, 1985). complexes phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate, decreased the production of inositol phosphates, partially prevented ptatelet aggregation induced by a high concentration of Cvx (10 nM) and abolished both platelet aggregation and inositol phosphate formation induced by thrombin (2 units/ml) and by a stable prostaglandin H2 analogue, U46619 (1 ,uM).…”

Section: Introductionmentioning

confidence: 98%

“…Since stimulation of platelets leads to the rapid degradation of inositol phospholipids (Billah and Lapetina, 1982; Morrison and Shukla, 1989), which are involved in further cell activation, we examined whether the effect of Cvx on platelets in-volves the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) by phosphoinositide-specific phospholipase C (PLC). The activation of PLC in washed rabbit platelets leads to the breakdown of inositol phospholipids and to the production of inositol 1,4,5trisphosphate (IP3), known to mobilize Ca21 from the endoplasmic reticulum to the cytosol (Streb et al, 1983;O'Rourke et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

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Convulxin-induced platelet aggregation is accompanied by a powerful activation of the phospholipase C pathway

Faili

Randon

Francischetti

et al. 1994

Biochemical Journal

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Platelet aggregation and stimulation of phosphoinositide-specific phospholipase C (PLC) by thrombin and by convulxin (Cvx), a non-enzymic snake venom glycoprotein, were compared. Cvx-stimulated production of inositol phosphates by washed platelets was independent of the cyclo-oxygenase pathway, formation of platelet-activating factor and ADP release, but prostacyclin (prostaglandin I2), a stimulator of cyclic AMP formation, suppressed its effects on platelet and PLC activation. Kinetic analysis showed that inositol 1,4,5-trisphosphate formation reached its maximal value 15 s after platelet stimulation with Cvx and persisted for at least 5 min. Neomycin sulphate (10 mM), which complexes phosphatidylinositol 4-phosphate and phosphatidyl-inositol 4,5-bisphosphate, decreased the production of inositol phosphates, partially prevented platelet aggregation induced by a high concentration of Cvx (10 nM) and abolished both platelet aggregation and inositol phosphate formation induced by thrombin (2 units/ml) and by a stable prostaglandin H2 analogue, U46619 (1 microM). In contrast with neomycin sulphate, Na2SO4 had no significant effect against all agonists tested. It is concluded that platelet activation by Cvx is partially mediated by PLC and involves other mechanisms as well.

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“…Based on the specific radioactivity of [32P]ATP determined as described in the Methods section and assuming that -8 x 108 platelets occupy a volume of 8 pl (Billah-& Lapetina, 1982), it -was calculated that after 60 s thrombin (0.2 units/ml) induces the intracellular formation of 20.2 + 6.3 /tM of lysophosphatidic acid and 154 + 4 /LM of phosphatidic acid (n = 3). The level of lysophosphatidic acid, therefore, is 13% of that of phosphatidic acid at this time.…”

Section: Thrombin-induced Formation Of Lysophosphatidic Acidmentioning

confidence: 99%

Decanoyl lysophosphatidic acid induces platelet aggregation through an extracellular action. Evidence against a second messenger role for lysophosphatidic acid

Watson¹,

McConnell²,

Lapetina³

1985

Biochemical Journal

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Platelets rapidly convert 1,2-didecanoyl-sn-glycerol into its corresponding phosphatidic acid and lysophosphatidic acid derivatives, thereby providing a means of introducing these two compounds into platelets. 1-Decanoyl-2-lyso-3-sn-phosphatidic acid, when added directly to platelets, induced platelet aggregation and raised intracellular Ca2+ levels at concentrations of 0.3 microM upwards, but was without effect when formed intracellularly from 1,2-didecanoylglycerol at an estimated concentration of approx. 47 microM. This indicates that the site of platelet activation by lysophosphatidic acid is extracellular. A concentration of thrombin (0.2 unit/ml), which produced maximal platelet aggregation, caused an estimated intracellular formation of 20 microM-lysophosphatidic acid in the presence of 2 mM-Ca2+; however, there was no detectable release of lysophosphatidic acid into the bathing medium. Lysophosphatidic acid, therefore, may not be an intracellular second messenger involved in platelet aggregation by thrombin.

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Rapid decrease of phosphatidylinositol 4,5-bisphosphate in thrombin-stimulated platelets.

Cited by 312 publications

References 38 publications

Biochemical studies on cell fusion. II. Control of fusion response by lipid alteration.

Biochemical studies on cell fusion. II. Control of fusion response by lipid alteration.

Convulxin-induced platelet aggregation is accompanied by a powerful activation of the phospholipase C pathway

Decanoyl lysophosphatidic acid induces platelet aggregation through an extracellular action. Evidence against a second messenger role for lysophosphatidic acid

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