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Sphingosine 1-phosphate breakdown in platelets
Yutaka Yatomi1, Soichiro Yamamura, Nobuo Hisano
1Department of Laboratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan. yatomiy-lab@h.u-tokyo.ac.jp
Journal of Biochemistry
|December 31, 2004
Summary
Platelets release sphingosine 1-phosphate (Sph-1-P), which dephosphorylates to initiate sphingolipid mediator formation. This pathway, involving extracellular Sph-1-P degradation, suggests a transmembrane cycling process in platelets.
Area of Science:
- Biochemistry
- Cell Biology
- Hematology
Background:
- Platelets are rich in sphingosine 1-phosphate (Sph-1-P), a key signaling molecule.
- Sphingolipid metabolism plays a crucial role in platelet function and extracellular signaling.
Purpose of the Study:
- To investigate the formation and extracellular release of sphingolipid mediators in activated platelets.
- To elucidate the role of sphingosine 1-phosphate (Sph-1-P) dephosphorylation in initiating sphingolipid signaling.
Main Methods:
- Platelet suspensions labeled with radioactive Sph were stimulated with thrombin or TPA.
- Sphingolipid levels (Sph-1-P, Sph, Cer, sphingomyelin) were quantified using HPLC.
- Sphingolipid phosphatase activity and extracellular Sph-1-P degradation were assessed.
Main Results:
- Platelet activation decreased Sph-1-P and increased Sph, Cer, and sphingomyelin.
- Sph-1-P dephosphorylation, not conversion to Cer or sphingomyelin, initiated mediator formation.
- Extracellular Sph-1-P was detected and degraded, suggesting ecto-phosphatase activity.
Conclusions:
- Platelets possess a transmembrane cycling pathway for sphingolipid mediator formation.
- Sph-1-P dephosphorylation is a critical initiating step in this pathway.
- Extracellular Sph-1-P may be rapidly degraded by platelet ecto-phosphatases.