ArticlePloS one2016
Partially Defective Store Operated Calcium Entry and Hem(ITAM) Signaling in Platelets of Serotonin Transporter Deficient Mice.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Immunothrombosis versus thrombo-inflammation: platelets in cerebrovascular complications.Research and practice in thrombosis and haemostasis · 2024Article
- Article
- New insights of platelet endocytosis and its implication for platelet function.Frontiers in cardiovascular medicine · 2023Review
- Novel salivary antihemostatic activities of long-form D7 proteins from the malaria vector Anopheles gambiae facilitate hematophagy.The Journal of biological chemistry · 2022Article
- Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022Review
- Microbiome-Related Indole and Serotonin Metabolites are Linked to Inflammation and Psychiatric Symptoms in People Living with HIV.International journal of tryptophan research : IJTR · 2022Article
- Serotonin: a platelet hormone modulating cardiovascular disease.Journal of thrombosis and thrombolysis · 2021Review
- Platelets as Modulators of Cerebral Ischemia/Reperfusion Injury.Frontiers in immunology · 2019Review
- Cangrelor Induces More Potent Platelet Inhibition without Increasing Bleeding in Resuscitated Patients.Journal of clinical medicine · 2018Article
- Calcium Signaling in Vertebrate Development and Its Role in Disease.International journal of molecular sciences · 2018Review
- Citalopram inhibits platelet function independently of SERT-mediated 5-HT transport.Scientific reports · 2018Article
- Dietary Sources and Bioactivities of Melatonin.Nutrients · 2017Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSerotonin (5-hydroxytryptamin, 5-HT) is an indolamine platelet agonist, biochemically derived from tryptophan. 5-HT is secreted from the enterochromaffin cells into the gastrointestinal tract and blood. Blood 5-HT has been proposed to regulate hemostasis by acting as a vasoconstrictor and by triggering platelet signaling through 5-HT receptor 2A (5HTR2A). Although platelets do not synthetize 5-HT, they take 5-HT up from the blood and store it in their dense granules which are secreted upon platelet activation.
objectiveTo identify the molecular composite of the 5-HT uptake system in platelets and elucidate the role of platelet released 5-HT in thrombosis and ischemic stroke.
methods5-HT transporter knockout mice (5Htt-/-) were analyzed in different in vitro and in vivo assays and in a model of ischemic stroke.
resultsIn 5Htt-/- platelets, 5-HT uptake from the blood was completely abolished and agonist-induced Ca2+ influx through store operated Ca2+ entry (SOCE), integrin activation, degranulation and aggregation responses to glycoprotein VI (GPVI) and C-type lectin-like receptor 2 (CLEC-2) were reduced. These observed in vitro defects in 5Htt-/- platelets could be normalized by the addition of exogenous 5-HT. Moreover, reduced 5-HT levels in the plasma, an increased bleeding time and the formation of unstable thrombi were observed ex vivo under flow and in vivo in the abdominal aorta and carotid artery of 5Htt-/- mice. Surprisingly, in the transient middle cerebral artery occlusion (tMCAO) model of ischemic stroke 5Htt-/- mice showed nearly normal infarct volume and the neurological outcome was comparable to control mice.
conclusionAlthough secreted platelet 5-HT does not appear to play a crucial role in the development of reperfusion injury after stroke, it is essential to amplify the second phase of platelet activation through SOCE and plays an important role in thrombus stabilization.
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