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Involvement of retinoic acid receptor-alpha-mediated signaling pathway in
induction of CD38 cell-surface antigen
K Mehta, T McQueen, T Manshouri, M Andreeff, S Collins and M Albitar
Department of Bioimmunotherapy, The University of Texas M.D. Anderson
Cancer Center, Houston 77030, USA.
Human leukocyte antigen CD38, a 45-kD single-chain, transmembrane
glycoprotein, is a bifunctional ectoenzyme that participates in signal
transduction pathways involved in the regulation of cell growth and
differentiation. In this study, we demonstrate the nature of retinoid
receptors involved in retinoic acid-induced expression of CD38 protein in
the human myeloblastic leukemia cell line HL-60. We used a variant HL-60
cell line, HL-60R, in which retinoid receptor function has been abrogated
by a trans-dominant negative mutation. We introduced the normal retinoic
acid receptors (RAR)-alpha, -beta, and -gamma or retinoid X receptor
(RXR)-alpha into HL-60R cells by retroviral vector- mediated gene transfer.
Based on experiments using these cell lines and receptor-specific synthetic
retinoids that preferentially bind to one of the RARs or RXRs, we conclude
that RAR-alpha is involved in retinoid- induced CD38 expression in HL-60
cells. Further evidence included our demonstration that blocking of
RAR-alpha with the antagonist Ro 41-5253 completely suppressed the
retinoid-induced expression of CD38 mRNA transcript and the production of
CD38 protein in HL-60 cells. Various tissues from transgenic mice that
expressed an antisense construct of RAR-alpha lacked or produced very low
levels of CD38. As expected, the tissues from transgenic mice contained 50%
to 80% reduced levels of RAR- alpha. These results suggest that regulation
of CD38 expression, both in vitro and in vivo, is under the direct control
of RAR-alpha retinoid receptors.
Volume 89,
Issue 10,
pp. 3607-3614,
05/15/1997
Copyright © 1997 by The American Society of Hematology
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