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Updated: Jul 28, 2025
Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells
Published on: December 27, 2017
Alterations in the megakaryocyte transcriptome impacts platelet function in sepsis and COVID-19 infection
Abigail Ajanel1, Elizabeth A Middleton2
1Molecular Medicine Program, University of Utah, Salt Lake City, UT 84112, USA; Department of Pathology, University of Utah, Salt Lake City, UT 84112, USA.
Abstract:
Platelets and their parent cell, the megakaryocyte (MK), are increasingly recognized for their roles during infection and inflammation. The MK residing in the bone marrow or arising from precursors trafficked to other organs for development go on to form platelets through thrombopoiesis. Infection, by direct and indirect mechanisms, can alter the transcriptional profile of MKs. The altered environment, whether mediated by inflammatory cytokines or other signaling mechanisms results in an altered platelet transcriptome. Platelets released into the circulation, in turn, interact with each other, circulating leukocytes and endothelial cells and contribute to the clearance of pathogens or the potentiation of pathophysiology through such mechanisms as immunothrombosis. In this article we hope to identify key contributions that explore the impact of an altered transcriptomic landscape during severe, systemic response to infection broadly defined as sepsis, and viral infections, including SARS-CoV2. We include current publications that outline the role of MKs from bone-marrow and extra-medullary sites as well as the circulating platelet. The underlying diseases result in thrombotic complications that exacerbate organ dysfunction and mortality. Understanding the impact of platelets on the pathophysiology of disease may drive therapeutic advances to improve the morbidity and mortality of these deadly afflictions.
Insights
Infection alters megakaryocyte (MK) and platelet transcriptomes, impacting immune responses and thrombosis. Understanding these changes is crucial for developing new treatments for severe infections like sepsis and viral diseases.
Area of Science:
- Hematology
- Immunology
- Infectious Diseases
Background:
- Megakaryocytes (MKs) and platelets play critical roles in infection and inflammation.
- Infection can alter the transcriptional profiles of MKs and circulating platelets.
- Altered platelet transcriptomes contribute to pathophysiology, including immunothrombosis.
Purpose of the Study:
- To explore the impact of altered transcriptomic landscapes in megakaryocytes and platelets during severe systemic infections.
- To review current literature on the role of MKs and platelets in sepsis and viral infections, including SARS-CoV-2.
- To highlight how these transcriptomic alterations contribute to thrombotic complications and mortality.
Main Methods:
- Review of current scientific literature on megakaryopoiesis, thrombopoiesis, and infection.
- Analysis of studies investigating transcriptomic changes in MKs and platelets during infection.
- Synthesis of information on the role of platelets in sepsis, viral infections, and immunothrombosis.
Main Results:
- Infections significantly alter the transcriptional profiles of bone marrow and extra-medullary megakaryocytes and circulating platelets.
- Altered platelets contribute to pathogen clearance or potentiation of pathophysiology via mechanisms like immunothrombosis.
- These transcriptomic changes are linked to thrombotic complications, exacerbating organ dysfunction and mortality in severe infections.
Conclusions:
- Understanding the altered transcriptomic landscape of MKs and platelets during severe infections is vital.
- Platelet-mediated mechanisms, including immunothrombosis, significantly impact disease severity and outcomes.
- Targeting these platelet-related pathways holds potential for therapeutic advancements to reduce morbidity and mortality in life-threatening infections.
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