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Blood, 15 October 2001, Vol. 98, No. 8, pp. 2563-2567
BRIEF REPORT
Lineage restriction of the RAR gene expression in
myeloid differentiation
Jun Zhu,
Clare M. Heyworth,
Annegret Glasow,
Qiu-Hua Huang,
Kevin Petrie,
Michel Lanotte,
Gérard Benoit,
Robert Gallagher,
Samuel Waxman,
Tariq Enver, and
Arthur Zelent
From the Leukaemia Research Fund Centre and Section of
Gene Function and Regulation at the Institute of Cancer Research,
Chester Beatty Laboratories, London, United Kingdom; CRC Section of
Haemopoietic Cell and Gene Therapeutics, Paterson Institute for Cancer
Research, Christie Hospital NHS Trust, Manchester, United Kingdom;
INSERM U496, Centre G. Hayem, Hôpital Saint-Louis, Paris, France;
Departments of Oncology and Medicine, Montefiore Medical Center and
Albert Einstein Cancer Center, Bronx, NY; and Division of Neoplastic
Diseases, Department of Medicine, Mount Sinai Medical Center, New York,
NY.
To better understand the role of retinoids in myelopoiesis,
expression of the retinoid receptor genes (retinoic acid receptors [RARs] and retinoid X receptors [RXRs]) were examined
during differentiation of factor-dependent cell-Paterson
(FDCP)-mixA4 murine progenitor cells. The major
receptor expressed in undifferentiated A4 cells was RAR (primarily
the RAR1 isoform). Following induction of myelomonocytic
differentiation with granulocyte and granulocyte-macrophage colony-stimulating factors, a dramatic increase in RAR
expression (particularly the RAR2 isoform) was seen. In contrast,
expression of both RAR isoforms was rapidly extinguished upon
induction of erythroid differentiation with erythropoeitin (EPO). A
modest induction of RXR expression was seen, particularly during
differentiation in the myelomonocytic lineage. Low expression levels of
RAR 2 and RXR remained unchanged, irrespective of differentiation
pathway. Consistent with the gene expression patterns, RAR agonists
and antagonists stimulated myelomonocytic and erythroid differentiation of FDCP-mixA4 cells, respectively. Taken together, these results suggest that erythropoiesis and granulopoiesis require diminished and
enhanced RAR activities, respectively, which at physiological all-trans-retinoic acid (RA) concentrations may be
accomplished by reciprocal effects of EPO and myelomonocytic growth
factors on its expression. This hypothesis is corroborated by data
showing that RA, which positively regulates RAR2 expression, can
exert inhibitory effects on erythroid differentiation.
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