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Publication : Low levels of erythroid and myeloid progenitors in thrombopoietin-and c-mpl-deficient mice.

First Author  Carver-Moore K Year  1996
Journal  Blood Volume  88
Issue  3 Pages  803-8
PubMed ID  8704234 Mgi Jnum  J:34532
Mgi Id  MGI:81988 Doi  10.1182/blood.v88.3.803.803
Citation  Carver-Moore K, et al. (1996) Low levels of erythroid and myeloid progenitors in thrombopoietin-and c-mpl-deficient mice. Blood 88(3):803-8
abstractText  Thrombopoietin (TPO), the ligand for the c-mpl receptor, has been shown to be the major regulator of platelet production. Mice deficient in either c-mpl or TPO generated by homologous recombination show a dramatic decrease in platelet counts, but other blood cell counts are normal. Because TPO treatment of myelosuppressed mice not only enhances the recovery of platelets but also accelerates erythroid recovery, we investigated the levels of myeloid and erythroid progenitor cells in TPO-or c-mpl-deficient mice. Our results show that the number of megakaryocyte, granulocyte-macrophage, erythroid, and multilineage progenitors are significantly reduced in the bone marrow, spleen, and peripheral blood of either TPO-or c-mpl-deficient mice. Administration of recombinant murine TPO to TPO-deficient mice and control littermate mice significantly increased the absolute number of myeloid, erythroid, and mixed progenitors in bone marrow and spleen. This increase was especially apparent in TPO-deficient mice where numbers were increased to a level greater than in diluent-treated control mice and approached or equaled that in the TPO-treated control mice. Moreover, TPO-administration greatly increased the number of circulating progenitors as well as platelets in both TPO-deficient and control mice. Furthermore, the megakaryocytopoietic activity of other cytokines in the absence of a functional TPO or c-mpl gene was shown both in vitro and in vivo.
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