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J. Biol. Chem., Vol. 275, Issue 50, 39747-39753, December 15, 2000
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From the Laboratory of Metabolism, NCI, National Institutes of
Health, Bethesda, Maryland 20892 and Aldehyde dehydrogenase 1 (ALDH1) plays a major
role in the biosynthesis of retinoic acid (RA), a hormone required for
several essential life processes. Recent evidence, using the aryl
hydrocarbon receptor-null mouse, suggests that elevated hepatic RA
down-regulates ALDH1 in a unique feedback pathway to control RA
biosynthesis. To determine the mechanism of suppression of the
ALDH1 gene by RA, transactivation studies were carried out
in Hepa-1 mouse hepatoma cells. RA decreased expression of an ALDH1-CAT
construct containing
Feedback Inhibition of the Retinaldehyde Dehydrogenase Gene
ALDH1 by Retinoic Acid through Retinoic Acid Receptor
and CCAAT/Enhancer-binding Protein 
*
, and NCI-Frederick
Cancer Research and Development Center,
Frederick, Maryland 21702-1201
2536 base pairs of DNA upstream of the
transcription start site. Retinoic acid receptor 
(RAR)
transactivates the ALDH1 gene promoter through a complex
with an RA response-like element (RARE) located at 91/75 bp, which
bound to the RAR/retinoid X receptor 
heterodimer.
CCAAT/enhancer-binding protein (C/EBP) also transactivates the
ALDH1 gene promoter through a CCAAT box located 3' and
directly adjacent to the RARE, and the ALDH1 gene is
down-regulated in C/EBP-null mouse liver. Exposure of Hepa-1 cells
to RA results in a decrease in C/EBP mRNA levels; however, there
was no difference in mRNA and protein levels between wild-type and
AHR-null mouse liver. These data support a model in which the RAR
and C/EBP activate the ALDH1 gene promoter through the
RARE and C/EBP response elements, and in Hepa-1 cells, high levels of
RA inhibit this activation by decreasing cellular levels of
C/EBP.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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