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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1264-1273
GATA-1 blocks IL-6-induced macrophage differentiation and
apoptosis through the sustained expression of cyclin D1 and Bcl-2 in a
murine myeloid cell line M1
Hirokazu Tanaka,
Itaru Matsumura,
Koichi Nakajima,
Hanako Daino,
Junko Sonoyama,
Hitoshi Yoshida,
Kenji Oritani,
Takashi Machii,
Masayuki Yamamoto,
Toshio Hirano, and
Yuzuru Kanakura
From the Departments of Hematology/Oncology, Internal Medicine II,
Molecular Oncology, Biomedical Research Center, Osaka University
Medical School, Osaka, Japan; the Department of Immunology, Osaka City
University Medical School, Japan; and the Center for TARA and Institute
of Basic Medical Institute, University of Tsukuba, Tsukuba, Japan.
Cytokines exert pleiotropic effects on target cells in a manner
dependent on the cell type or stage of differentiation. To determine
how instinctive cell properties affect biological effects of cytokine,
we introduced an erythroid/megakaryocyte lineage-specific transcription
factor, GATA-1, into a murine myeloid cell line M1, which is known to
undergo macrophage differentiation in response to interleukin 6 (IL-6).
Overexpression of GATA-1 changed the phenotype of M1 cells from myeloid
to megakaryocytic lineage. Furthermore, GATA-1 blocked both
IL-6-induced macrophage differentiation and apoptosis of M1 cells.
Although STAT3 is essential for IL-6-induced macrophage differentiation
of M1 cells, GATA-1 had little or no effect on tyrosine
phosphorylation, DNA binding, and transcriptional activities of STAT3
in Western blot analysis, electropholic mobility shift
assay (EMSA), and luciferase assays. During IL-6-induced macrophage
differentiation of M1 cells, IL-6 down-regulated cyclin D1 expression
and induced p19INK4D expression, leading to reduction in
cdk4 activities. In contrast, sustained expression of cyclin D1 and a
significantly lesser amount of p19INK4D induction were
observed in IL-6-treated M1 cells overexpressing GATA-1. Furthermore,
although bcl-2 expression was severely reduced by IL-6 in M1 cells, it
was sustained in GATA-1-introduced M1 cells during the culture with
IL-6. Both IL-6-induced macrophage differentiation and apoptosis were
significantly abrogated by coexpression of cyclin D1 and bcl-2, whereas
overexpressions of cyclin D1 or bcl-2 inhibited only differentiation or
apoptosis, respectively. These results suggested that GATA-1 may not
only reprogram the lineage phenotype of M1 cells but also disrupt the biologic effects of IL-6 through the sustained expression of cyclin D1
and bcl-2.
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