ArticleBlood2015
Myosin-II repression favors pre/proplatelets but shear activation generates platelets and fails in macrothrombocytopenia.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Role of the nonhelical tailpiece of myosin-II in regulating filament architecture and function.The Journal of cell biology · 2026Article
- Optimizing the Method for Differentiation of Functional Platelets from Human Induced Pluripotent Stem Cells.Stem cell reviews and reports · 2026Article
- [The application of thrombopoietin receptor agonists in the treatment of non-muscle myosin heavy chain 9-related disease].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Lipid droplets are rigid and physically suppress phagocytosis, unless cell compression or stretching activates actomyosin.Molecular biology of the cell · 2026Article
- Integrating the Study of Polyploidy Across Organisms, Tissues, and Disease.Annual review of genetics · 2024Review
- Megakaryocyte-induced contraction of plasma clots: cellular mechanisms and structural mechanobiology.Blood · 2024Article
- Contractility defects hinder glycoprotein VI-mediated platelet activation and affect platelet functions beyond clot contraction.Research and practice in thrombosis and haemostasis · 2024Article
- Matrix stiffness controls megakaryocyte adhesion, fibronectin fibrillogenesis, and proplatelet formation through Itgβ3.Blood advances · 2023Article
- The Importance of Alpha-Actinin Proteins in Platelet Formation and Function, and Their Causative Role in Congenital Macrothrombocytopenia.International journal of molecular sciences · 2021Review
- Cytoskeletal-based mechanisms differently regulateHaematologica · 2021Article
- Role of Thrombopoietin Receptor Agonists in Inherited Thrombocytopenia.International journal of molecular sciences · 2021Review
- Latest culture techniques: cracking the secrets of bone marrow to mass-produce erythrocytes and plateletsHaematologica · 2021Review
- Flow-accelerated platelet biogenesis is due to an elasto-hydrodynamic instability.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- T-lymphocyte passive deformation is controlled by unfolding of membrane surface reservoirs.Molecular biology of the cell · 2016Article
- A potential role for genome structure in the translation of mechanical force during immune cell development.Nucleus (Austin, Tex.) · 2016Review
- Inherited thrombocytopenia: novel insights into megakaryocyte maturation, proplatelet formation and platelet lifespan.Platelets · 2016Review
- Nuclear lamins in cancer.Cellular and molecular bioengineering · 2016Article
- Megakaryocytic Maturation in Response to Shear Flow Is Mediated by the Activator Protein 1 (AP-1) Transcription Factor via Mitogen-activated Protein Kinase (MAPK) Mechanotransduction.The Journal of biological chemistry · 2016Article
- Defects in TRPM7 channel function deregulate thrombopoiesis through altered cellular Mg(2+) homeostasis and cytoskeletal architecture.Nature communications · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Megakaryocyte ploidy and the generation of pre/proplatelets are both increased in culture by pharmacologic inhibition of myosin-II, but nonmuscle myosin-IIA (MIIA) mutations paradoxically cause MYH9-related diseases (MYH9-RD) that adversely affect platelets. In marrow, megakaryocytes extend projections into the microcirculation, where shear facilitates fragmentation to large pre/proplatelets, suggesting that fluid stresses and myosin-II activity somehow couple in platelet biogenesis. Here, in bulk shear, plateletlike particles generated from megakaryocytes are maximized at a shear stress typical of that in the microcirculation and after treatment with a myosin-II inhibitor. MIIA activity in static cells is naturally repressed through phosphorylation at Serine-1943, but shear decreases phosphorylation, consistent with MIIA activation and localization to platelet cortex. Micropipette aspiration of cells shows myosin-II accumulates at stressed sites, but its inhibition prevents such mechanoactivation and facilitates generation of CD41(+) fragments similar in size to pre/proplatelets. MYH9-RD mutants phenocopy inhibition, revealing a dominant negative effect. MIIA is diffuse in the large platelets of a MYH9-RD patient with macrothrombocytopenia and is also diffuse in normal pre/proplatelets treated with inhibitor that blocks in vitro division to small platelets. The findings explain the large platelets in MYH9-RD and the near-normal thrombocrit of patients. Myosin-II regulation thus controls platelet size and number.
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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.