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Blood, Vol. 95 No. 11 (June 1), 2000:
pp. 3349-3356
Vitamin A deficiency in mice causes a systemic
expansion of myeloid cells
Takeshi Kuwata,
I-Ming Wang,
Tomohiko Tamura,
Roshini M. Ponnamperuma,
Rachel Levine,
Kevin L. Holmes,
Herbert C. Morse III,
Luigi M. De
Luca, and
Keiko Ozato
From the Laboratory of Molecular Growth Regulation, National
Institute of Child Health and Human Development; the Laboratory of
Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute;
and the Flow Cytometry Unit and Laboratory of Immunopathology, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, Bethesda, MD
To examine the role of retinoids in hematopoietic cell growth in
vivo, we studied female SENCAR mice made vitamin A deficient by dietary
restriction. Deficient mice exhibited a dramatic increase in myeloid
cells in bone marrow, spleen, and peripheral blood. The abnormal
expansion of myeloid cells was detected from an early stage of vitamin
A deficiency and contrasted with essentially normal profiles of T and B
lymphocytes. This abnormality was reversed on addition of retinoic acid
to the vitamin A-deficient diet, indicating that the myeloid cell
expansion is a direct result of retinoic acid deficiency. TUNEL
analysis indicated that spontaneous apoptosis, a normal process in the
life cycle of myeloid cells, was impaired in vitamin A-deficient mice,
which may play a role in the increased myeloid cell population.
Quantitative reverse transcriptase-polymerase chain reaction analysis
of purified granulocytes showed that expression of not only RAR, but
RXRs, 2 nuclear receptors that mediate biologic activities of
retinoids, was significantly reduced in cells of deficient mice. This
work shows that retinoids critically control the homeostasis of myeloid
cell population in vivo and suggests that deficiency in this signaling
pathway may contribute to various myeloproliferative disorders.
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