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Sphingosine 1-Phosphate Produced by Sphingosine Kinase 2 Intrinsically Controls Platelet Aggregation In Vitro and In

Nicole Urtz1, Florian Gaertner1, Marie-Luise von Bruehl1

  • 1From the Medizinische Klinik und Poliklinik I, Klinikum der Universität München (N.U., F.G., M.-L.v.B., S.C., F.R., M.O., V.B., J.B., I.S., M.L., K.R.L., S.M.), Department of Applied Physics, Center for NanoSciences (K.R.L.), and Walther-Straub-Institute of Pharmacology and Toxicology (M.M.y.S.), Ludwig-Maximilians-Universität, Munich, Germany; DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany (N.U., F.G., M.-L.v.B., S.C., F.R., M.O., J.B., I.S., M.L., M.M.y.S., S.M.); Heart Failure Institute, Research Center for Translational Medicine and Department of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China (L.Z.); Institute of Pharmacology, University of Bern, Bern, Switzerland (A.H.); Pharmazentrum Frankfurt/ZAFES, Goethe University Hospital, Frankfurt am Main, Germany (J.M.P.); and Preclinical Safety (D.L., E.P.), and Autoimmunity, Transplantation and Inflammation (C.B., A.B., T.B.), Novartis Institutes for BioMedical Research, Basel, Switzerland.

Circulation Research
|July 2, 2015
PubMed
Summary

Sphingosine kinase 2 (Sphk2) is critical for generating sphingosine 1-phosphate (S1P) in platelets, regulating their aggregation and arterial thrombus stability. Sphk2 deficiency protects mice from thrombosis without affecting bleeding.

Keywords:
blood plateletsplatelet aggregationsphingosine 1-phosphatesphingosine kinasethrombosis

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Area of Science:

  • Biochemistry
  • Hematology
  • Pharmacology

Background:

  • Platelets are vital for hemostasis.
  • Sphingosine kinases (Sphk) 1 and 2 produce sphingosine 1-phosphate (S1P).
  • The intrinsic role of S1P in platelet function is largely unknown.

Purpose of the Study:

  • To investigate the role of Sphk1- and Sphk2-derived S1P in regulating platelet function.
  • To elucidate the mechanism by which S1P influences platelet activation.

Main Methods:

  • Mass spectrometry to quantify intracellular S1P levels in Sphk2(-/-) platelets.
  • Whole blood impedance aggregometry to assess platelet aggregation.
  • Intravital microscopy to evaluate in vivo arterial thrombus stability.

Main Results:

  • Sphk2(-/-) platelets showed a 100-fold reduction in S1P levels and failed to secrete S1P upon stimulation.
  • Sphk2-deficient mice exhibited decreased platelet aggregation and reduced arterial thrombus stability.
  • S1P regulates platelet aggregation via the sphingosine 1-phosphate receptor 1.

Conclusions:

  • Sphk2 is the primary Sphk isoform for S1P generation in platelets, intrinsically controlling platelet activation.
  • Sphk2-deficient mice are protected from arterial thrombosis but maintain normal bleeding times.
  • Targeting the Sphk2-S1P pathway offers a potential therapeutic strategy for preventing thrombosis.