G-CSF administration results in thrombocytopenia by inhibiting differentiation of hematopoietic progenitors into megakaryocytes.

In this study, we investigated the effects of G-CSF on platelet counts in healthy mice and mice that received bone marrow transplantation. It was observed that G-CSF administration induced thrombocytopenia in healthy mice and aggravated thrombocytopenia in mice that received bone marrow transplantation. Furthermore, we analyzed the regulatory effects of G-CSF on the differentiation of hematopoietic progenitors and megakaryocytes, and activation of platelets and endothelial cells. The results reveal that G-CSF administration causes thrombocytopenia mainly by inhibiting the differentiation of common myeloid progenitors and megakaryotic erythroid progenitors into megakaryocytes and platelet formation but not through enhancing activation of platelets or endothelial cells and following platelet consumption. Collectively, G-CSF administration can result in thrombocytopenia in hematopoietic stem cell donors and exacerbate existing thrombocytopenia in transplantation recipients. More attention should be paid to bleeding risk of G-CSF administration in HSCT, especially autologous HSCT. PMID: 31473203 [PubMed - as supplied by publisher]
Source: Biochemical Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Biochem Pharmacol Source Type: research