Transforming growth factor beta 1 systemically modulates granuloid, erythroid, lymphoid, and thrombocytic cells in mice
Carlino, J.A.; Higley, H.R.; Creson, J.R.; Avis, P.D.; Ogawa, Y.; Ellingsworth, L.R.
Experimental Hematology 20(8): 943-950
1992
ISSN/ISBN: 0301-472X PMID: 1505639 Document Number: 403069
Transforming growth factor .beta.1 (TGF-.beta.1) has been shown to inhibit the development of most early hemopoietic progenitors in vitro. The present series of in vivo experiments show that TGF-.beta.1 can simultaneously augment and suppress distinct cell lineages in peripheral and central hemopoietic compartments. Mice treated daily for 7-14 days with s.c. injections of TGF-.beta.1 exhibited up to a 95% reduction in circulating platelets and a 50% reduction in red cell counts, whereas a 50-400% increase occurred in circulating white cells with the morphology of small lymphocytes. Decreased erythrocytes were also evident in the splenic red pulp and bone marrow sinusoids. A dramatic increase in granulopoiesis occurred in the spleen and bone marrow, followed by a peripheral neutrophilia 1 week after treatments ceased. All effects were completely reversible, with normal histologic and hematologic profiles evident 2 weeks after cessation of treatments. Thus, TGF-.beta.1 can differentially regulate multiple hemopoietic pathways in a systemic, reversible, and dose-dependent fashion. These actions may be mediated by the direct effects of TGF-.beta.1 or through modulation of secondary cytokines and receptors.