Co-activation of Gi and Gq proteins exerts synergistic effect on human platelet aggregation through activation of phospholipase C and Ca2+ signalling pathways

Shah, Bukhtiar H.; Siddiqui, A. M.; Qureshi, Kamran; Khan, Mojammel A.; Rafi, S; Ujan, V A; Yakoob, M Y; Rasheed, Huma; Saeed, Sheikh A.

doi:10.1038/emm.1999.7

Cited by 36 publications

(25 citation statements)

References 23 publications

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“…Verapamil is well-documented calcium antagonist with regard to antiplatelet effects having the most varied possible mechanisms of action (Hjemdahl and Wallen, 1997). Our previous studies show that synergistic effect of various platelet agonists is blocked by calcium-channel blockers, verapamil and diltiazem in very low concentration Shah et al, 1999;. Similarly the present findings also show that PAF and A23187 mediated platelet aggregation is also blocked by low concentration of verapamil or diltiazem.…”

Section: Discussionsupporting

confidence: 67%

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

Rasheed

Saeed²

2004

Exp Mol Med

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Section: Discussionsupporting

confidence: 67%

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

Rasheed

Saeed²

2004

Exp Mol Med

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“…Aggregation was monitored using a Dualchannel Lumi Aggregometer (Model 400 Chronolog Corporation, Chicago, USA) using 0.45 mL aliquots of PRP (Shah et al, 1999). The final volume was made up to 0.5 mL with the test drug dissolved either in normal saline or appropriate vehicle known to be devoid of any effect on aggregation.…”

Section: Measurement Of Platelet Aggregationmentioning

confidence: 99%

Ethnopharmacological studies on antispasmodic and antiplatelet activities of Ficus carica

Gilani

Mehmood

Janbaz

et al. 2008

Journal of Ethnopharmacology

117

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“…For example, G␣ i/oor G␣ s -coupled receptors can markedly enhance the Ca 2ϩ signaling of simultaneously activated G␣ q/11 -coupled receptors in clonal cell lines (Dickenson and Hill, 1994;Yeo et al, 2001). Such cross talk has also been demonstrated in cells derived from both the central nervous system (Jimenez et al, 1999;Hirono et al, 2001) and peripheral tissues (Shah et al, 1999;Cilluffo et al, 2000;Buckley et al, 2001) where potentiated cellular Ca 2ϩ signaling may have important physiological consequences (Buckley et al, 2001;Hirono et al, 2001).…”

mentioning

confidence: 93%

Cross Talk between P2Y₂Nucleotide Receptors and CXC Chemokine Receptor 2 Resulting in Enhanced Ca²⁺Signaling Involves Enhancement of Phospholipase C Activity and Is Enabled by Incremental Ca²⁺Release in Human Embryonic Kidney Cells

Werry

Wilkinson²,

Willars³

2003

J Pharmacol Exp Ther

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We have shown previously that activation of endogenously expressed, G␣ q/11 -coupled P2Y 2 nucleotide receptors with UTP reveals an intracellular Ca 2ϩ response to activation of recombinant, G␣ i -coupled CXC chemokine receptor 2 (CXCR2) in human embryonic kidney cells. Here, we characterize further this cross talk and demonstrate that phospholipase C (PLC) and inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ]-dependent Ca 2ϩ release underlies this potentiation. The putative Ins(1,4,5)P 3 receptor antagonist 2-aminoethoxydiphenyl borane reduced the response to CXCR2 activation by interleukin-8, as did sustained inhibition of phosphatidylinositol 4-kinase with wortmannin, suggesting the involvement of phosphoinositides in the potentiation. Against a Li ϩ block of inositol monophosphatase activity, costimulation of P2Y 2 nucleotide receptors and CXCR2 caused phosphoinositide accumulation that was significantly greater than that after activation of P2Y 2 nucleotide receptors or CXCR2 alone, and was more than additive. Thus, PLC activity, as well as Ca 2ϩ release, was enhanced. In these cells, agonist-mediated Ca 2ϩ release was incremental in nature, suggesting that a potentiation of Ins(1,4,5)P 3 generation in the presence of coactivation of P2Y 2 nucleotide receptors and CXCR2 would be sufficient for additional Ca 2ϩ release. Potentiated Ca 2ϩ signaling by CXCR2 was markedly attenuated by expression of either regulator of G protein signaling 2 or the G␤␥-scavenger G␣ t1 (transducin ␣ subunit), indicating the involvement of G␣ q and G␤␥ subunits, respectively.Through a variety of intracellular signal transduction pathways, diverse ligands of G protein-coupled receptors (GPCRs) are able to regulate many different aspects of cell function. Typically, each GPCR is considered to preferentially activate a specific signal transduction pathway, but it is clear that promiscuity and cross talk can occur. Thus, a GPCR may couple to more than one pathway, whereas activation of a GPCR is often able to influence the signaling by another coexpressed receptor. Such cross talk can have either positive or negative effects on receptor function and may serve to allow coincidence detection, thereby integrating signals from multiple receptor types.A phenomenon of particular interest in terms of positive GPCR cross talk is the enhancement of intracellular Ca 2ϩ release arising as a consequence of the concomitant or sequential stimulation of two types of GPCR that are preferentially coupled to different G proteins. For example, G␣ i/oor G␣ s -coupled receptors can markedly enhance the Ca 2ϩ signaling of simultaneously activated G␣ q/11 -coupled receptors in clonal cell lines (Dickenson and Hill, 1994;Yeo et al., 2001). Such cross talk has also been demonstrated in cells derived from both the central nervous system (Jimenez et al., 1999;Hirono et al., 2001) and peripheral tissues (Shah et al., This work was jointly funded by the Biotechnology and Biological Sciences Research Council and AstraZeneca R&D Charnwood (Loughborough, UK)....

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Co-activation of Gi and Gq proteins exerts synergistic effect on human platelet aggregation through activation of phospholipase C and Ca2+ signalling pathways

Abstract: Abstract

Cited by 36 publications

References 23 publications

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

Ethnopharmacological studies on antispasmodic and antiplatelet activities of Ficus carica

Cross Talk between P2Y₂Nucleotide Receptors and CXC Chemokine Receptor 2 Resulting in Enhanced Ca²⁺Signaling Involves Enhancement of Phospholipase C Activity and Is Enabled by Incremental Ca²⁺Release in Human Embryonic Kidney Cells

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Co-activation of Gi and Gq proteins exerts synergistic effect on human platelet aggregation through activation of phospholipase C and Ca2+ signalling pathways

Abstract: Abstract

Cited by 36 publications

References 23 publications

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

Ethnopharmacological studies on antispasmodic and antiplatelet activities of Ficus carica

Cross Talk between P2Y2Nucleotide Receptors and CXC Chemokine Receptor 2 Resulting in Enhanced Ca2+Signaling Involves Enhancement of Phospholipase C Activity and Is Enabled by Incremental Ca2+Release in Human Embryonic Kidney Cells

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Cross Talk between P2Y₂Nucleotide Receptors and CXC Chemokine Receptor 2 Resulting in Enhanced Ca²⁺Signaling Involves Enhancement of Phospholipase C Activity and Is Enabled by Incremental Ca²⁺Release in Human Embryonic Kidney Cells