Stefan Engelhardt, MD, PhD, Institut für Pharmakologie und Toxikologie, Technische Universität München, Biedersteiner Strasse 29, 80802 Munich, Germany, Tel.: +49 89 4140 3260, E-mail:
Thromb Haemost. 2013 Dec;110(6):1207-14. doi: 10.1160/TH13-07-0623. Epub 2013 Sep 26.
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.
微小 RNA（miRNAs）是多种细胞类型中关键的生理调节因子。在这里，我们评估了 miR-223 缺失小鼠的血小板生成和功能，miR-223 是血小板和巨核细胞中表达最丰富的 miRNA 之一。我们发现 miR-223 缺失小鼠的血小板数量、大小、寿命以及血小板黏附受体的表面表达均无变化。同样，miR-223 的缺失也不影响血小板的激活、黏附和聚集，也不影响出血时间。此外，miR-223 缺失的巨核细胞正常发育，并能够形成前血小板。然而，我们在 miR-223 缺失动物中，抗体诱导的血小板耗竭后，血小板数量的恢复出现短暂延迟。在将 miR-223 缺失动物的骨髓移植到野生型受体中后，没有观察到这种延迟，这表明 miR-223 在血栓生成中具有非细胞自主的作用。总的来说，我们的数据表明 miR-223 在血小板生成中的作用令人惊讶地较小，而血小板的功能似乎不依赖于 miR-223。
