ArticleHaematologica2026
Thyroid hormones induce an acute platelet release mechanism via integrin αVβ3.
Article in Haematologica, 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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Abstract
Understanding how mature megakaryocytes release their platelets and, crucially, what are the triggers that facilitate this process is of huge impact on human medicine. Controlling this biological process, as well as being able to utilize platelets produced in vitro will be a major therapeutic advancement. Unfortunately, the exact mechanism and mediators that drive thrombopoiesis remain elusive. Here, we seek to identify such mediators through studying the dynamics of platelet production after an acute loss of platelets. Analysis of plasma taken from 19 plateletpheresis donors at various timepoints before and after donation identified peak platelet production timepoints (4-8 hours). Analysis of these timepoints by proteomic and metabolomic techniques enabled the identification of triiodothyronine (T3), as well as its analogs, GC-1 (sobetirome), MGL-3196 (resmetirom) and KB2115 (eprotirome), as having a direct effect on in vitro platelet production in human cord blood (fold-change at 12 hours, mean ± standard deviation [SD]: T3 3 hours 100 nM, 1.26±0.24; GC-1 100 μM, 5.54±1.58; MGL-3196 300 μM, 6.92±1.38; KB2115 75 μM, 17.90±5.25) and induced pluripotent stem cell-derived megakaryocytes (foldchange, mean ± SD: viral A1ATD1 KB2115 36.1 μM, 3.36±0.38; inducible QOLG1.1H KB2115 75 μM, 1.85±0.46). Receptor-specific antagonists revealed that thyroid hormone-induced platelet production primarily signals via a non-genomic signaling pathway, integrin αVβ3 (CD51/61, vitronectin receptor), which megakaryocytes express highly. When combined with silk-based three-dimensional scaffold bioreactor technology, we observed a significant upscaling of platelets (fold-change, mean ± SD: KB2115, 2.8±0.79) that responded positively to agonist stimulation (P-selectin exposure). This shows the direct impact of thyroid hormones on platelet production through integrin αVβ3, which offers interesting therapeutic potential in the field of transfusion medicine.
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