ArticleAmerican journal of physiology. Cell physiology2014
Sphingosine kinase 1 (Sphk1) negatively regulates platelet activation and thrombus formation.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Exploration of the Sphingolipid Metabolite, Sphingosine-1-phosphate and Sphingosine, as Novel Biomarkers for Aspirin-exacerbated Respiratory Disease.Scientific reports · 2016Trial
- S1P receptor 1 signaling reduces arterial thrombosis via up-regulation of endothelial thrombomodulin expression.Science advances · 2026Article
- Article
- Identification of Hub Genes for Dexmedetomidine Alleviation of Limb Ischemia-Reperfusion-Induced Lung Injury in Rats by Transcriptomic.Journal of inflammation research · 2025Article
- Sphingosine-1-phosphate modulates PAR1-mediated human platelet activation in a concentration-dependent biphasic manner.Scientific reports · 2021Article
- The Role of Chemoprophylactic Agents in Modulating Platelet Aggregability After Traumatic Brain Injury.The Journal of surgical research · 2019Article
- Sphingolipid dysregulation due to lack of functional KDSR impairs proplatelet formation causing thrombocytopenia.Haematologica · 2019Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingosine 1-phosphate (S1P) is a powerful regulator of platelet formation. Enzymes generating S1P include sphingosine kinase 1. The present study thus explored the role of sphingosine kinase 1 in platelet formation and function. Activation-dependent platelet integrin αIIbβ3 activation and secretion of platelets lacking functional sphingosine kinase 1 (sphk1(-/-)) and of wild-type platelets (sphk1(+/+)) were determined utilizing flow cytometry and chronolume luciferin assay. Cytosolic Ca(2+) activity ([Ca(2+)]i) and aggregation were measured using fura-2 fluorescence and aggregometry, respectively. In vitro platelet adhesion and thrombus formation were evaluated using a flow chamber with shear rates of 1,700 s(-1). Activation-dependent increase of [Ca(2+)]i, degranulation (release of alpha and dense granules), integrin αIIbβ3 activation, and aggregation were all significantly increased in sphk1(-/-) platelets compared with sphk1(+/+) platelets. Moreover, while platelet adhesion and thrombus formation under arterial shear rates were significantly augmented in Sphk1-deficient platelets, bleeding time and blood count were unaffected in sphk1(-/-) mice. In conclusion, sphingosine kinase 1 is a powerful negative regulator of platelet function counteracting degranulation, aggregation, and thrombus formation.
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