ArticleHaematologica2021
Desialylation of
Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Clinical application of a modified platelet desialylation test for mechanistic characterization of platelet transfusion refractoriness.Transfusion · 2026Article
- Platelet CLEC-2 activation leads to GPIb⍺ shedding: Implications for doxorubicin chemotherapy and thrombosis.The Journal of biological chemistry · 2026Article
- Hematopoietic Aging and Leukemia: Mechanistic and Therapeutic Insights.International journal of molecular sciences · 2026Review
- Comparative phenotyping of surface markers and glycans in murine and human platelet-derived extracellular vesicles.Research and practice in thrombosis and haemostasis · 2026Article
- Thrombocytopenia: from physiological homeostasis imbalance to mechanism-driven precision diagnosis and therapy.Frontiers in immunology · 2026Review
- Kupffer cells are essential for platelet-mediated thrombopoietin generation in the liver.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- The role of platelet desialylation as a biomarker in primary immune thrombocytopenia: mechanisms and therapeutic perspectives.Frontiers in immunology · 2024Review
- Specific O-glycans in the mechanosensory domain of glycoprotein Ibα are important for its stability and function.Haematologica · 2023Article
- Shear-Mediated Platelet Microparticles Demonstrate Phenotypic Heterogeneity as to Morphology, Receptor Distribution, and Hemostatic Function.International journal of molecular sciences · 2023Article
- Comprehensive analysis of platelet glycoprotein Ibα ectodomain glycosylation.Journal of thrombosis and haemostasis : JTH · 2023Article
- Inherited Thrombocytopenia Caused by Variants in Crucial Genes for Glycosylation.International journal of molecular sciences · 2023Review
- Signaling mechanisms of the platelet glycoprotein Ib-IX complex.Platelets · 2022Review
- Overlapping and unique substrate specificities of ST3GAL1 and 2 during hematopoietic and megakaryocytic differentiation.Blood advances · 2022Article
- Novel Therapies to Address Unmet Needs in ITP.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Fast clearance of platelets in a commonly used mouse model for GPIbα is impeded by an anti-GPIbβ antibody derivative.Journal of thrombosis and haemostasis : JTH · 2022Article
- The GPIb-IX complex on platelets: insight into its novel physiological functions affecting immune surveillance, hepatic thrombopoietin generation, platelet clearance and its relevance for cancer development and metastasis.Experimental hematology & oncology · 2022Review
- Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation.International journal of molecular sciences · 2022Review
- GPIbα is the driving force of hepatic thrombopoietin generation.Research and practice in thrombosis and haemostasis · 2021Article
- The Provocative Roles of Platelets in Liver Disease and Cancer.Frontiers in oncology · 2021Review
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
During infection neuraminidase desialylates platelets and induces their rapid clearance from circulation. The underlying molecular basis, particularly the role of platelet glycoprotein (GP)Ibα therein, is not clear. Utilizing genetically altered mice we report that the extracellular domain of GPIbα, but neither von Willebrand factor nor ADAM17 (a disintegrin and metalloprotease 17), is required for platelet clearance induced by intravenous injection of neuraminidase. Lectin binding to platelets following neuraminidase injection over time revealed that the extent of desialylation of O-glycans correlates with the decrease of platelet count in mice. Injection of α2,3-neuraminidase reduces platelet counts in wild-type but not in transgenic mice expressing only a chimeric GPIbα that misses most of its extracellular domain. Neuraminidase treatment induces unfolding of the O-glycosylated mechanosensory domain in GPIbα as monitored by single-molecule force spectroscopy, increases the exposure of the ADAM17 shedding cleavage site in the mechanosensory domain on the platelet surface, and induces ligand-independent GPIb-IX signaling in human and murine platelets. These results suggest that desialylation of O-glycans of GPIbα induces unfolding of the mechanosensory domain, subsequent GPIb-IX signaling including amplified desialylation of N-glycans, and eventually rapid platelet clearance. This new molecular mechanism of GPIbα-facilitated clearance could potentially resolve many puzzling and seemingly contradicting observations associated with clearance of desialylated or hyposialylated platelets.
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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.