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Prepublished online as a Blood First Edition Paper on August 29, 2002; DOI 10.1182/blood-2001-11-0084.
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Blood, 15 January 2003, Vol. 101, No. 2, pp. 524-531
HEMATOPOIESIS
Tumor necrosis factor-alpha expressed constitutively in erythroid
cells or induced by erythropoietin has negative and stimulatory
roles in normal erythropoiesis and erythroleukemia
Sarah M. Jacobs-Helber,
Kwan-ho Roh,
Daniel Bailey,
Emmanuel N. Dessypris,
John J. Ryan,
Jingchun Chen,
Amittha Wickrema,
Dwayne L. Barber,
Paul Dent, and
Stephen T. Sawyer
From the Departments of Pharmacology/Toxicology,
Radiation Oncology and Physiology, Medical College of Virginia Campus;
the Department of Biology, Virginia Commonwealth University; and the
Department of Internal Medicine, Hunter Holmes McGuire Veterans
Administration Medical Center, Richmond, VA; and the Division of
Cellular and Molecular Biology, Ontario Cancer Institute, University
Health Network, Toronto, Ontario, Canada.
Binding of erythropoietin (EPO) to its receptor (EPOR) on erythroid
cells induces the activation of numerous signal transduction pathways,
including the mitogen-activated protein kinase Jun-N-terminal kinase
(JNK). In an effort to understand the regulation of EPO-induced proliferation and JNK activation, we have examined the role of potential autocrine factors in the proliferation of the murine erythroleukemia cell line HCD57. We report here that treatment of these
cells with EPO induced the expression and secretion of tumor necrosis
factor alpha (TNF- ). EPO-dependent proliferation was reduced by the
addition of neutralizing antibodies to TNF-, and exogenously added
TNF- induced proliferation of HCD57 cells. EPO also could induce
TNF- expression in BAF3 and DA3 myeloid cells ectopically expressing
EPOR. Addition of TNF- activated JNK in HCD57 cells, and the
activity of JNK was partially inhibited by addition of a TNF-
neutralizing antibody. Primary human and murine erythroid progenitors
expressed TNF- in either an EPO-dependent or constitutive manner.
However, TNF- had an inhibitory effect on both immature primary
human and murine cells, suggestive that the proliferative effects of
TNF- may be limited to erythroleukemic cells. This study suggests a
novel role for autocrine TNF- expression in the proliferation of
erythroleukemia cells that is distinct from the effect of TNF- in
normal erythropoiesis.
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