ArticleBlood cells, molecules & diseases
Morphological and functional platelet abnormalities in Berkeley sickle cell mice.
Article in Blood cells, molecules & diseases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- NLRP3 inflammasome-mediated platelet hyperreactivity in sickle cell mice is targetable by BTK inhibition.Biochemical and biophysical research communications · 2026Article
- High-mobility group box 1 increases platelet surface P2Y12 and platelet activation in sickle cell disease.JCI insight · 2024Article
- Mouse models of sickle cell disease: Imperfect and yet very informative.Blood cells, molecules & diseases · 2024Review
- Intra-erythrocytic vacuoles in asplenic patients: elusive genesis and original clearance of unique organelles.Frontiers in physiology · 2023Review
- Sickle Cell Disease: A Paradigm for Venous Thrombosis Pathophysiology.International journal of molecular sciences · 2020Review
- Application of the automated haematology analyzer XN-30 in an experimental rodent model of malaria.Malaria journal · 2018Article
- Photoacoustic Flow Cytometry for Single Sickle Cell DetectionAnalytical cellular pathology (Amsterdam) · 2016Article
- Article
- In vivo assessment of rodent Plasmodium parasitemia and merozoite invasion by flow cytometry.Journal of visualized experiments : JoVE · 2015Article
- A flow cytometric assay to quantify invasion of red blood cells by rodent Plasmodium parasites in vivo.Malaria journal · 2014Article
- Article
- Mechanisms of enhanced thrombus formation in cerebral microvessels of mice expressing hemoglobin-S.Blood · 2011Article
- P-selectin-mediated platelet-neutrophil aggregate formation activates neutrophils in mouse and human sickle cell disease.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Berkeley sickle cell mice are used as animal models of human sickle cell disease but there are no reports of platelet studies in this model. Since humans with sickle cell disease have platelet abnormalities, we studied platelet morphology and function in Berkeley mice (SS). We observed elevated mean platelet forward angle light scatter (FSC) values (an indirect measure of platelet volume) in SS compared to wild type (WT) (37+/-3.2 vs. 27+/-1.4, mean+/-SD; p<0.001), in association with moderate thrombocytopenia (505+/-49 x 10(3)/microl vs. 1151+/-162 x 10(3)/microl; p<0.001). Despite having marked splenomegaly, SS mice had elevated levels of Howell-Jolly bodies and "pocked" erythrocytes (p<0.001 for both) suggesting splenic dysfunction. SS mice also had elevated numbers of thiazole orange positive platelets (5+/-1% vs. 1+/-1%; p<0.001), normal to low plasma thrombopoietin levels, normal plasma glycocalicin levels, normal levels of platelet recovery, and near normal platelet life spans. Platelets from SS mice bound more fibrinogen and antibody to P-selectin following activation with a threshold concentration of a protease activated receptor (PAR)-4 peptide compared to WT mice. Enlarged platelets are associated with a predisposition to arterial thrombosis in humans and some humans with SCD have been reported to have large platelets. Thus, additional studies are needed to assess whether large platelets contribute either to pulmonary hypertension or the large vessel arterial occlusion that produces stroke in some children with sickle cell disease.
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