MiR-223 is dispensable for platelet production and function in mice

Thromb Haemost. 2013 Dec;110(6):1207-14. doi: 10.1160/TH13-07-0623. Epub 2013 Sep 26.

Abstract

MicroRNAs (miRNAs) are key physiological regulators in multiple cell types. Here, we assessed platelet production and function in mice deficient in miR-223, one of the most abundantly expressed miRNAs in platelets and megakaryocytes. We found platelet number, size, life-span as well as surface expression of platelet adhesion receptors to be unchanged in miR-223-deficient mice. Likewise, loss of miR-223 did not affect platelet activation, adhesion and aggregation and also had no effect on bleeding times. Moreover, miR-223 null megakaryocytes developed normally and were capable to form pro-platelets. However, we detected a transient delay in the recovery of platelet numbers following antibody-induced platelet depletion in miR-223-deficient animals. This delay was not observed after transplantation of bone marrow from miR-223-deficient animals into wild-type recipients, indicating a non-cell-autonomous role of miR-223 for thrombopoiesis. Overall, our data indicate a surprisingly modest role of miR-223 in platelet production, while the function of platelets does not seem to depend on miR-223.

Keywords: MicroRNA; megakaryocytes; platelets; transgenic mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibody-Dependent Cell Cytotoxicity / genetics
  • Bleeding Time
  • Blood Coagulation / genetics
  • Blood Platelets / physiology*
  • Bone Marrow Transplantation
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Cell Count
  • Cells, Cultured
  • Humans
  • Megakaryocytes / physiology*
  • Mice
  • Mice, Inbred Strains
  • Mice, Knockout
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Platelet Activation / genetics
  • Thrombopoiesis / genetics
  • Transplantation Chimera

Substances

  • Cell Adhesion Molecules
  • MIRN223 microRNA, mouse
  • MicroRNAs