ArticleProteoglycan research2025
Platelet Hyaluronan Synthase 3 Regulates Thrombin Signaling and Adhesion to Fibrinogen Under Venous Shear.
Article in Proteoglycan research, 2025. 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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Abstract
Hyaluronan (HA) is an essential glycosaminoglycan with supportive roles in hematopoiesis. HA is synthesized by hyaluronan synthases (HAS1, HAS2, and HAS3) and plays a crucial role in cellular signaling and extracellular matrix interactions. Megakaryocytes (MKs), the platelet progenitor cell, express only HAS2 and HAS3, and dysregulated metabolism of HA by MKs leads to thrombocytopenia. To unravel the contribution of HAS3 in platelet function, Using HAS1/3 knockout (dKO) mice, we demonstrate that thrombin-mediated activation is significantly impaired, whereas collagen-dependent activation remains intact. Functional assays indicate that platelet aggregation, integrin α
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