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Mice and mouse platelets are major experimental models for hemostasis and thrombosis; however, important physiological data from this model has received little to no quantitative, 3D ultrastructural analysis. We used state-of-the-art, serial block imaging scanning electron microscopy (SBF-SEM, nominal Z-step size was 35 nm) to image resting platelets from C57BL/6 mice. α-Granules were identified morphologically and rendered in 3D space. The quantitative analysis revealed that mouse α-granules typically had a variable, elongated, rod shape, different from the round/ovoid shape of human α-granules. This variation in length was confirmed qualitatively by higher-resolution, focused ion beam (FIB) SEM at a nominal 5 nm Z-step size. The unexpected α-granule shape raises novel questions regarding α-granule biogenesis and dynamics. Does the variation arise at the level of the megakaryocyte and α-granule biogenesis or from differences in α-granule dynamics and organelle fusion/fission events within circulating platelets? Further quantitative analysis revealed that the two major organelles in circulating platelets, α-granules and mitochondria, displayed a stronger linear relationship between organelle number/volume and platelet size, i.e., a scaling in number and volume to platelet size, than found in human platelets suggestive of a tighter mechanistic regulation of their inclusion during platelet biogenesis. In conclusion, the overall spatial arrangement of organelles within mouse platelets was similar to that of resting human platelets, with mouse α-granules clustered closely together with little space for interdigitation of other organelles.
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http://dx.doi.org/10.1080/09537104.2020.1799970 | DOI Listing |
Int J Toxicol
September 2025
Department of Cardiology, Fuwai Yunnan Hospital, Chinese Academy of Medical Sciences, Affiliated Cardiovascular Hospital of Kunming Medical University, Kunming, China.
Platelet hyperactivation represents a significant risk factor for atherosclerotic cardiovascular diseases. This study investigated the expression and functional roles of integrin αvβ3 and (Multimerin 1) MMRN1 in platelets from atherosclerotic conditions and evaluated the therapeutic potential of integrin αvβ3 antagonism in atherosclerotic progression. We examined the expression patterns of αvβ3 and MMRN1 in platelets from healthy controls, patients with coronary heart disease (CHD), and patients with acute myocardial infarction (AMI) using qRT-PCR and ELISA techniques.
View Article and Find Full Text PDFBlood
September 2025
University of Illinois at Chicago, Chicago, Illinois, United States.
Hematopoietic stem cells (HSCs) responsible for blood cell production and their bone marrow regulatory niches undergo age-related changes, impacting immune responses and predisposing individuals to hematologic malignancies. Here, we show that the age-related alterations of the megakaryocytic niche and associated downregulation of Platelet Factor 4 (PF4) are pivotal mechanisms driving HSC aging. PF4-deficient mice display several phenotypes reminiscent of accelerated HSC aging, including lymphopenia, increased myeloid output, and DNA damage, mimicking physiologically aged HSCs.
View Article and Find Full Text PDFBlood Vessel Thromb Hemost
August 2025
Hematology, Thrombosis and Hemostasis Research Program, Versiti Blood Research Institute, Wauwatosa, WI.
Unopposed platelet activation can be associated with pathologic thrombosis. An intact growth arrest-specific gene 6 (GAS6)/Mer receptor tyrosine kinase (MERTK) signaling pathway contributes importantly to potentiating platelet activation triggered by molecular agonists ex vivo and thrombus stabilization in vivo. We describe, herein, the inhibition of platelet function and stable thrombus formation conferred by iMer, a naturally occurring MERTK splice variant, that acts as a GAS6 decoy receptor and decreases phosphorylation of MERTK.
View Article and Find Full Text PDFPlatelets
December 2025
Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada.
The integrin family of extracellular matrix (ECM) adhesion receptors plays a central role in platelet function, including adhesion and aggregation. In resting platelets, integrins exist in a low-affinity state for their ligands, and are activated upon ligand binding to the extracellular domain or binding of cytoplasmic proteins such as talin to the intracellular β-tail. Talin function is regulated through autoinhibition, which reduces its integrin-activating function.
View Article and Find Full Text PDFJ Thromb Haemost
September 2025
Key Laboratory of Thrombosis and Hemostasis of National Health Commission, Jiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, Suzhou, China; Engineering Center of Hematological Disease of Ministry of Education, Cyrus Tang Hematology Center, Collaborative Innovation
Background: Megakaryocyte (MK) fragmentation into proplatelets (PPTs) and microparticles (MKMPs) is well established, yet the mechanisms underlying MKMP generation remain unclear.
Objectives: In order to investigate the role of integrin β3 and cytoskeletal dynamics during megakaryopoiesis and explore potential therapeutic targets for thrombocytopenia.
Methods: Proplatelet formation and MKMP release were evaluated both in vivo and in vitro under integrin β3 receptor impaired environment.