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The Journal of Immunology, Vol 156, Issue 3 939-947, Copyright © 1996 by American Association of Immunologists
ARTICLES |
C Minshall, S Arkins, GG Freund and KW Kelley
Department of Animal Sciences, University of Illinois, Urbana 61801, USA.
Hemopoietic growth factors promote survival of progenitor cells by preventing their apoptotic death. Recently, phosphatidylinositol 3'- kinase (PI 3-kinase) has been shown to be integral in the pathway by which insulin and nerve growth factor prevent apoptosis. In this work, we show that IL-3-dependent FDCP-1/Mac-1 murine hemopoietic progenitors express receptors for another growth factor, insulin-like growth factor- I (IGF-I), and that both IL-3 and IGF-I stimulate PI 3-kinase activity. We then demonstrate that IGF-I shares with IL-3 the properties of significantly promoting proliferation and enhancing survival of myeloid progenitor cells at concentrations as low as 3 ng/ml. IL-3 and IGF-I efficiently promote cell survival in the presence of inhibitors of either RNA synthesis (actinomycin D) or mitosis (mitomycin C), suggesting that both ligands promote survival by a process that is largely independent of RNA synthesis. To determine whether PI 3-kinase mediates IL-3- and IGF-I-induced inhibition of apoptosis, FDCP-1/Mac-1 cells were incubated with the PI 3-kinase inhibitor, wortmannin. While wortmannin inhibited both basal and IGF-I- and IL-3-induced PI 3-kinase enzyme activity, it did not affect the ability of IL-3 to protect FDCP- 1/Mac-1 cells from apoptosis, even though it abrogated the IGF-I- induced inhibition of apoptosis. These data demonstrate that even though activation of PI 3-kinase is a pleiotropic feature of both IL-3 and IGF-I receptors in myeloid progenitors, prevention of apoptosis by IL-3 but not IGF-I is independent of PI 3-kinase. Survival of hemopoietic progenitors is therefore maintained by at least two different intracellular signaling pathways, one requiring PI 3-kinase and one that does not.
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H.-P. Gerber, A. McMurtrey, J. Kowalski, M. Yan, B. A. Keyt, V. Dixit, and N. Ferrara Vascular Endothelial Growth Factor Regulates Endothelial Cell Survival through the Phosphatidylinositol 3'-Kinase/Akt Signal Transduction Pathway. REQUIREMENT FOR Flk-1/KDR ACTIVATION J. Biol. Chem., November 13, 1998; 273(46): 30336 - 30343. [Abstract] [Full Text] [PDF]
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M. Pap and G. M. Cooper Role of Glycogen Synthase Kinase-3 in the Phosphatidylinositol 3-Kinase/Akt Cell Survival Pathway J. Biol. Chem., August 7, 1998; 273(32): 19929 - 19932. [Abstract] [Full Text] [PDF]
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J.-R. Chao, J.-M. Wang, S.-F. Lee, H.-W. Peng, Y.-H. Lin, C.-H. Chou, J.-C. Li, H.-M. Huang, C.-K. Chou, M.-L. Kuo, et al. mcl-1 Is an Immediate-Early Gene Activated by the Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) Signaling Pathway and Is One Component of the GM-CSF Viability Response Mol. Cell. Biol., August 1, 1998; 18(8): 4883 - 4898. [Abstract] [Full Text]
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Q. Liu, W. Ning, R. Dantzer, G. G. Freund, and K. W. Kelley Activation of Protein Kinase C-{zeta} and Phosphatidylinositol 3'-Kinase and Promotion of Macrophage Differentiation by Insulin-Like Growth Factor-I J. Immunol., February 1, 1998; 160(3): 1393 - 1401. [Abstract] [Full Text] [PDF]
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Y. M. Li, D. H. Schacher, Q. Liu, S. Arkins, N. Rebeiz, R. H. McCusker Jr., R. Dantzer, and K. W. Kelley Regulation of Myeloid Growth and Differentiation by the Insulin-Like Growth Factor I Receptor Endocrinology, January 1, 1997; 138(1): 362 - 368. [Abstract] [Full Text] [PDF]
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P. Erhardt and G. M. Cooper Activation of the CPP32 Apoptotic Protease by Distinct Signaling Pathways with Differential Sensitivity to Bcl-xL J. Biol. Chem., July 26, 1996; 271(30): 17601 - 17604. [Abstract] [Full Text] [PDF]
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