Trial reportMolecular and cellular biochemistry2017
Flow cytometric analysis reveals the high levels of platelet activation parameters in circulation of multiple sclerosis patients.
Trial report in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The research landscape and evolutionary trends of platelet-derived extracellular vesicles: a bibliometric and LDA analysis (2015-2026).Frontiers in oncology · 2026Pooled it
- Influence of cardiopulmonary exercise test on platelet function in patients with coronary artery diseases on antiplatelet therapy.BMC cardiovascular disorders · 2022Trial
- Impact of Whole-Body Cryostimulation (WBC) on Hemostatic Parameters in Patients with Multiple Sclerosis.Journal of clinical medicine · 2026Article
- Molecular regulatory mechanisms of depression-related thrombosis risk.Journal of medical biochemistry · 2025Article
- Article
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- Hematological markers as prognostic indicators in multiple sclerosis progression.Biomarkers in medicine · 2025Article
- Oxymatrine, a novel TLR2 agonist, promotes megakaryopoiesis and thrombopoiesis through the STING/NF-κB pathway.Journal of pharmaceutical analysis · 2025Article
- The Role of Extracellular Vesicles and Microparticles in Central Nervous System Disorders: Mechanisms, Biomarkers, and Therapeutic Potential.Cellular and molecular neurobiology · 2024Review
- Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression?Journal of neuroinflammation · 2024Review
- Pathogenic Role of Fibrinogen in the Neuropathology of Multiple Sclerosis: A Tale of Sorrows and Fears.Neurochemical research · 2023Review
- Targeting TLR2/Rac1/cdc42/JNK Pathway to Reveal That Ruxolitinib Promotes Thrombocytopoiesis.International journal of molecular sciences · 2022Article
- Multiple sclerosis and genetic polymorphisms in fibrinogen-mediated hemostatic pathways: a case-control study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Article
- Preparations from selected cucurbit vegetables as antiplatelet agents.Scientific reports · 2021Article
- The Molecular Aspects of Disturbed Platelet Activation through ADP/P2YInternational journal of molecular sciences · 2021Article
- Anti-Platelet Properties of Phenolic and Nonpolar Fractions Isolated from Various Organs ofInternational journal of molecular sciences · 2021Article
- The Impact of SARS-CoV-2 Infection on the Development of Neurodegeneration in Multiple Sclerosis.International journal of molecular sciences · 2021Review
- The Role of Platelets in the Stimulation of Neuronal Synaptic Plasticity, Electric Activity, and Oxidative Phosphorylation: Possibilities for New Therapy of Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Increased Pro-Thrombotic Platelet Activity Associated with Thrombin/PAR1-Dependent Pathway Disorder in Patients with Secondary Progressive Multiple Sclerosis.International journal of molecular sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epidemiological studies confirm an increased risk of cardiovascular disease in multiple sclerosis, especially prothrombotic events directly associated with abnormal platelet activity. The aim of our study was to investigate the level of blood platelet activation in the circulation of patients with chronic phase of multiple sclerosis (SP MS) and their reactivity in response to typical platelets' physiological agonists. We examined 85 SP MS patients diagnosed according to the revised McDonald's criteria and 50 healthy volunteers as a control group. The platelet activation and reactivity were assessed using flow cytometry analysis of the following: P-selectin expression (CD62P), activation of GP IIb/IIIa complex (PAC-1 binding), and formation of platelet microparticles (PMPs) and platelet aggregates (PA) in agonist-stimulated (ADP, collagen) and unstimulated whole blood samples. Furthermore, we measured the level of soluble P-selectin (sP-selectin) in plasma using ELISA method, to evaluate the in vivo level of platelet activation, both in healthy and SP MS subjects. We found a statistically significant increase in P-selectin expression, GP IIb/IIIa activation, and formation of PMPs and PA, as well as in unstimulated and agonist-stimulated (ADP, collagen) platelets in whole blood samples from patients with SP MS in comparison to the control group. We also determined the higher sP-selectin level in plasma of SP MS subjects than in the control group. Based on the obtained results, we might conclude that during the course of SP MS platelets are chronically activated and display hyperreactivity to physiological agonists, such as ADP or collagen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.