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Updated: Mar 29, 2026

Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells
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CCL5 derived from platelets increases megakaryocyte proplatelet formation.

Kellie R Machlus1, Kelly E Johnson1, Rajesh Kulenthirarajan2

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Summary

Platelets release chemokine ligand 5 (CCL5) that signals through CCR5 on megakaryocytes, boosting platelet production during physiological stress. This mechanism may explain reactive thrombocytosis.

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Area of Science:

  • Hematology
  • Immunology
  • Cell Biology

Background:

  • Reactive thrombocytosis, a rise in platelet count during physiological stress, is poorly understood.
  • Platelets store and release inflammatory cytokines, including chemokine ligand 5 (CCL5).

Purpose of the Study:

  • To investigate the role of platelet-derived CCL5 in regulating megakaryocyte (MK) proplatelet production and platelet count during stress.

Main Methods:

  • Treatment of MKs with platelet releasate and recombinant CCL5.
  • Use of CCR5 antagonist (Maraviroc) and CCL5 immunodepletion.
  • Assessment of proplatelet formation, MK ploidy, and Akt signaling pathway.
  • In vivo study using a murine acute colitis model.

Main Results:

  • Platelet releasate significantly increased MK proplatelet production.
  • CCL5 and its receptor CCR5 mediate this effect, as shown by Maraviroc and CCL5 depletion.
  • Recombinant CCL5 increased proplatelet formation and MK ploidy in a CCR5-dependent manner.
  • CCL5/CCR5 signaling may suppress apoptosis via the Akt pathway.
  • In vivo, Maraviroc treatment abolished the correlation between platelet count and inflammation.

Conclusions:

  • Platelet-derived CCL5 signaling through CCR5 on MKs is a key mechanism driving increased platelet production during physiological stress.
  • This pathway contributes to reactive thrombocytosis and may be a therapeutic target.