ArticleResearch square2026
Early emergence of contractility and mechanotransduction during human megakaryopoiesis.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
6 authors.
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Abstract
The ability to contract blood clots is a hallmark of functional platelets. Proteins that support agonist-induced platelet contraction are expressed in megakaryocytes (MKs) and transferred to platelets during thrombopoiesis. Here, we investigated when during MK development the functional machinery for contraction emerges. Human induced pluripotent stem cells (iPSCs) were differentiated into embryonic hematopoietic progenitor cells (HPCs) and further matured into MKs (iMKs) to map the emergence of contractility and mechanotransduction across differentiation. Expression of total (CD41) and activated (mAb PAC-1) αIIbβ3 integrin, the thrombin receptor PAR1, and the MK marker CD42b was quantified by flow cytometry. Cell contractility was assessed by optically tracking human plasma clot shrinkage following thrombin stimulation. Undifferentiated iPSCs lacked detectable αIIbβ3 and were non-contractile. Both HPCs and iMKs exhibited agonist-induced contractility, integrin activation, and force transmission to extracellular fibrin, although at different levels. Following thrombin stimulation, activated αIIbβ3 on the cell surface was approximately 5-fold lower in HPCs and restricted to the MK-committed CD42b
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