ArticleThrombosis and haemostasis2012
Farnesyl pyrophosphate is an endogenous antagonist to ADP-stimulated P2Y₁₂ receptor-mediated platelet aggregation.
Article in Thrombosis and haemostasis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Effects of uridine and nucleotides on hemostasis parameters.Journal of thrombosis and thrombolysis · 2023Article
- Microglia and Neuroinflammation: What Place for P2RY12?International journal of molecular sciences · 2021Review
- Blood cells: an historical account of the roles of purinergic signalling.Purinergic signalling · 2015Review
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8 authors at 1 institution in 1 country.
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Abstract
Farnesyl pyrophosphate (FPP) is an intermediate in cholesterol biosynthesis, and it has also been reported to activate platelet LPA (lysophosphatidic acid) receptors. The aim of this study was to investigate the role of extracellular FPP in platelet aggregation. Human platelets were studied with light transmission aggregometry, flow cytometry and [³⁵S]GTPγS binding assays. As shown previously, FPP could potentiate LPA-stimulated shape change. Surprisingly, FPP also acted as a selective insurmountable antagonist to ADP-induced platelet aggregation. FPP inhibited ADP-induced expression of P-selectin and the activated glycoprotein (Gp)IIb/IIIa receptor. FPP blocked ADP-induced inhibition of cAMP accumulation and [³⁵S]GTPγS binding in platelets. In Chinese hamster ovary cells expressing the P2Y₁₂ receptor, FPP caused a rightward shift of the [³⁵S]GTPγS binding curve. In Sf9 insect cells expressing the human P2Y₁₂ receptor, FPP showed a concentration-dependent, although incomplete inhibition of [³H]PSB-0413 binding. Docking of FPP in a P2Y₁₂ receptor model revealed molecular similarities with ADP and a good fit into the binding pocket for ADP. In conclusion, FPP is an insurmountable antagonist of ADP-induced platelet aggregation mediated by the P2Y₁₂ receptor. It could be an endogenous antithrombotic factor modulating the strong platelet aggregatory effects of ADP in a manner similar to the use of clopidogrel, prasugrel or ticagrelor in the treatment of ischaemic heart disease.
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