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Blood, 1 April 2002, Vol. 99, No. 7, pp. 2379-2386
HEMATOPOIESIS
Retinoid signaling regulates primitive (yolk sac)
hematopoiesis
Satish Ghatpande,
Ashwini Ghatpande,
Justin Sher,
Maija H. Zile, and
Todd Evans
From the Department of Developmental and Molecular
Biology, Albert Einstein College of Medicine, Bronx, NY; and the
Department of Food Science and Human Nutrition, Michigan State
University, East Lansing.
It is known from nutritional studies that vitamin A is an important
factor for normal hematopoiesis, though it has been difficult to define
its precise role. The vitamin A-deficient (VAD) quail embryo provides
an effective ligand "knockout" model for investigating the function
of retinoids during development. The VAD embryo develops with a
significant reduction in erythroid cells, which has not been noted
previously. Activation of the primitive erythroid program and early
expression of the erythroid marker GATA-1 occurs, though GATA-1 levels
eventually decline, consistent with the erythropoietic and hemoglobin
deficits. However, from its early stages, the GATA-2 gene
fails to be expressed normally in VAD embryos. The bone morphogenetic protein (BMP)-signaling pathway regulates GATA-2, and BMP4 expression becomes reduced in the caudal embryonic region of VAD embryos. Adding
BMP4 to cultured VAD-derived explants rescues the production of
erythroid cells, whereas normal embryos cultured in the presence of the
BMP antagonist noggin are defective in primitive hematopoiesis. We find
that cell clusters of primitive blood islands undergo an inappropriate
program of apoptosis in the VAD embryo, which can explain the deficit
in differentiated primitive blood cells. We propose that vitamin
A-derived retinoids are required for normal yolk sac hematopoiesis and
that an embryonic retinoid-BMP-GATA-2 signaling pathway controls
progenitor cell survival relevant to primitive hematopoiesis.
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