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Blood, 1 February 2002, Vol. 99, No. 3, pp. 746-753
PLENARY PAPER
The cytokines IL-3 and GM-CSF regulate the transcriptional
activity of retinoic acid receptors in different in vitro models of
myeloid differentiation
Barton S. Johnson,
LeMoyne Mueller,
Jutong Si, and
Steven J. Collins
From the Division of Hospital Dentistry, University of
Washington, and the Human Biology Division, Fred Hutchinson Cancer
Research Center, Seattle, WA.
The disruption of retinoic acid receptor (RAR) activity that
characterizes human acute promyelocytic leukemia (APL) is associated with a block to granulocytic differentiation indicating that RARs are
critical regulators of normal myeloid differentiation. Nevertheless, how RAR activity might be regulated in the presumably homogenous concentration of retinoids in blood and bone marrow and how these receptors might interact with specific hematopoietic cytokines to
regulate normal myeloid differentiation remain unclear. Here, using
several cytokine-dependent in vitro models of myeloid development, it
was observed that specific hematopoietic cytokines that
normally regulate myeloid lineage commitment and differentiation
(interleukin-3 and granulocyte-macrophage colony-stimulating factor)
trigger the enhancement of both ligand-dependent and ligand-independent transcriptional activity of both endogenous and exogenous (transiently transfected) RARs. This cytokine-mediated enhancement of RAR activity is not associated with any observed changes in expression of the RARs
or their respective coactivators/corepressors. These studies define a
previously unknown cytokine-RAR interaction during myelopoiesis and
suggest that RAR activation might be a critical downstream event
following interleukin-3 and granulocyte-macrophage colony-stimulating factor signaling during myeloid differentiation. This observation of
ligand-independent activation of RARs that is mediated by certain cytokines represents a new paradigm with respect to how RAR activity might be modulated during hematopoiesis and also suggests a molecular basis for the differential sensitivity of human acute myelogenous leukemia cells to retinoids.
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