A glycoprotein VI signaling defect in newly formed platelets generated in stress thrombopoiesis
In this study, we report a functional defect in platelet GPVI signaling present in multiple models of thrombocytopenia that are accompanied by an increased proportion of rapidly generated young platelets. These results indicate that during stress thrombopoiesis, the GPVI receptor becomes entirely functional only after spending some time in circulation.
Authors
- Stephanie R. Hyslop (ORCID: https://orcid.org/0000-0001-5006-1627)
- Amanda E. Au (ORCID: https://orcid.org/0000-0003-3656-2673)
- Pradnya Gangatirkar
- Marion Lebois
- Jason Corbin
- Elizabeth E. Gardiner (ORCID: https://orcid.org/0000-0001-9453-9688)
- Diane Moujalled (ORCID: https://orcid.org/0000-0002-6405-2788)
- Irina Pleines (ORCID: https://orcid.org/0000-0002-9959-8174)
- Emma C. Josefsson (ORCID: https://orcid.org/0000-0001-6478-5204)
- Warren S. Alexander (ORCID: https://orcid.org/0000-0002-1824-7701)
- Robert K. Andrews (ORCID: https://orcid.org/0000-0001-9577-8082)
Institutions
- Australian National University (AU)
- The University of Melbourne (AU)
- Walter and Eliza Hall Institute of Medical Research (AU)
Publication Details
- Journal
- Journal of Thrombosis and Haemostasis
- Published
- 2025-03-06
- DOI
- https://doi.org/10.1016/j.jtha.2025.02.035
- Citations
- 2
- Primary Topic
- Platelet Disorders and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 3.54
Funders
- University of Melbourne
- Department of Health, State Government of Victoria
- Lorenzo and Pamela Galli Charitable Trust
- Medical Research Council
- National Health and Medical Research Council