HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints/Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Metcalf, D. Articles by Di Rago, L. Search for Related Content PubMed PubMed Citation Articles by Metcalf, D. Articles by Di Rago, L.

Murine Megakaryocyte Progenitor Cells and Their Susceptibility to Suppression by G-CSF

Division of Cancer and Hematology, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia

Key Words. Megakaryocyte colonies • G-CSF • Suppression

Correspondence: Donald Metcalf, Division of Cancer and Hematology, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia. Telephone: 61-3-9345-2555; fax: 61-3-9347-0852; e-mail: metcalf{at}wehi.edu.au

In agar cultures of mouse bone marrow cells, mega-karyocyte colony-forming cells exhibited shorter survival times than granulocyte-macrophage progenitor cells when initially cultured in the absence of stimulating factors. Initiation of cultures with G-CSF improved the survival times of granulocyte-macrophage progenitor cells and those of megakaryocyte progenitor cells. Paradoxically, G-CSF was found to consistently inhibit megakaryocyte colony formation stimulated by erythropoietin or by stem cell factor plus interleukin-3 (IL-3) plus erythropoietin. G-CSF was a less-consistent inhibitor of megakaryocyte colonies stimulated by thrombopoietin or IL-3. Analysis of the response of marrow cells from mice with the deletion of the genes encoding CIS, SOCS-1, SOCS-2, SOCS-3, SOCS-5, SOCS-6, or SOCS-7 indicated that the inhibitory SOCS proteins, with the possible exception of SOCS-3, were not involved in the G-CSF–initiated suppression of megakaryocyte colony formation.