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Blood, 1 March 2001, Vol. 97, No. 5, pp. 1314-1320
HEMATOPOIESIS
Positive and negative regulation of granulopoiesis by
endogenous RAR
Philippe Kastner,
H.
Jeffrey Lawrence,
Caroline Waltzinger,
Norbert B. Ghyselinck,
Pierre Chambon, and
Susan Chan
From the Institut de
Génétique et de Biologie Moléculaire et Cellulaire,
Illkirch, France.
Acute promyelocytic leukemia (APL) is always associated with
chromosomal translocations that disrupt the retinoic acid
receptor  (RAR) gene. Whether these
translocations relate to a role for endogenous RAR in normal
granulopoiesis remains uncertain because most studies addressing this
question have used non-physiological overexpression systems.
Granulocyte differentiation in cells derived from
RAR-deficient (RAR /) mice was studied and
evaluated in the context of agonist-bound and ligand-free RAR. Our
results demonstrate that RAR is dispensable for granulopoiesis, as
RAR/ mice have a normal granulocyte population
despite an impaired ability to respond to retinoids. However, although
it is not absolutely required, RAR can bidirectionally modulate
granulopoiesis. RAR stimulates differentiation in response to
exogenous retinoic acid. Furthermore, endogenous retinoids
control granulopoiesis in vivo, as either vitamin A-deficient
mice or animals treated with an RAR antagonist accumulate more immature
granulocytes in their bone marrow. Conversely, RAR acts to limit
differentiation in the absence of ligand because granulocyte precursors
from RAR/ mice differentiate earlier in culture.
Thus, the block in granulopoiesis exerted by RAR fusion proteins
expressed in APL cells may correspond to an amplification of a
normal function of unliganded RAR.
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