Abstract
The bloodstream typically contains >500 billion anucleate circulating platelets, derived from megakaryocytes in the bone marrow. This review will focus on two interesting aspects of bone marrow dysfunction and how this impacts on the quality of circulating platelets. In this regard, although megakaryocytes are from the myeloid lineage leading to granulocytes (including neutrophils), erythrocytes, and megakaryocytes/platelets, recent evidence has shown that defects in the lymphoid lineage leading to B cells, T cells, and natural killer (NK) cells also result in abnormal circulating platelets. Current evidence is limited regarding whether this latter phenomenon might potentially arise from (a) some form of as-yet-undetected defect common to both lineages; (b) adverse interactions occurring between cells of different lineages within the bone marrow environment; and/or (c) unknown disease-related factor(s) affecting circulating platelet receptor expression/function after their release from megakaryocytes. Understanding the mechanisms underlying how both myeloid and lymphoid lineage bone marrow defects lead to dysfunction of circulating platelets is significant because of the potential diagnostic and predictive value of peripheral platelet analysis for bone marrow disease progression, the additional potential effects of new anti-cancer drugs on platelet function, and the critical role platelets play in regulation of bleeding risk, inflammation, and innate immunity.
Highlights
The bloodstream typically contains >500 billion circulating anucleate platelets (~150–400 × 109 /L in ~4–5 L of blood) derived from megakaryocytes primarily situated in the bone marrow
While platelet GPVI-related dysfunction is associated with a significant proportion of myelodysplastic syndrome (MDS) cases, further studies are no doubt required to fully evaluate these changes temporally and in response to treatment in order to discover the molecular link between specific defects and platelet function, and to establish any prognostic value in future
Current evidence is limited regarding whether the effect of chronic lymphocytic leukemia (CLL)-related defects on circulating platelet profile might potentially result from (a) some form of as-yet-undetected defect common to both lineages; (b) adverse interactions occurring between cells of different lineages within the bone marrow environment; and/or (c) unknown disease-related factor(s) affecting circulating platelet receptor expression/function after their release from megakaryocytes
Summary
The bloodstream typically contains >500 billion circulating anucleate platelets (~150–400 × 109 /L in ~4–5 L of blood) derived from megakaryocytes primarily situated in the bone marrow. While platelet GPVI-related dysfunction is associated with a significant proportion of MDS cases, further studies are no doubt required to fully evaluate these changes temporally and in response to treatment in order to discover the molecular link between specific defects and platelet function, and to establish any prognostic value in future.
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