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J. Biol. Chem., Vol. 276, Issue 16, 12697-12701, April 20, 2001
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From the Renal Bioengineering Unit, Department of Medicine, Royal
Free and University College Medical School, University College London,
Jules Thorn Institute, Middlesex Hospital, Motimer Street, London W1T
3AA, United Kingdom
Retinoic acids exert profound effects on
many biological processes including cell proliferation,
differentiation, and morphogenesis. We previously reported that
all-trans-retinoic acid (t-RA) protected mesangial cells
from H2O2-triggered apoptosis by
suppressing the activator protein 1 (AP-1) pathway. It was via
inhibition of c-fos and c-jun expression
and suppression of c-Jun N-terminal kinase (JNK) activation. In this
report, we investigated the involvement of retinoic acid receptor (RAR)
and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in
H2O2-exposed cells. We found that pretreatment
with RAR pan-antagonist (AGN193109) or RXR pan-antagonist (HX531)
attenuated the antiapoptotic effect of t-RA. Similarly,
transient transfection with a dominant-negative mutant of RAR or a
dominant-negative RXR diminished the antiapoptotic effect of t-RA. Both
RAR and RXR antagonists reversed the suppressive effect of t-RA on AP-1
activity. However, the roles of RAR and RXR in the suppression of AP-1
components by t-RA were found to be different. RAR antagonist reversed
the suppressive effect of t-RA on both c-fos and
c-jun, whereas RXR antagonist reversed the effect of t-RA
on c-fos but not c-jun. Furthermore,
suppression of JNK activation by t-RA was observed even in the presence
of RAR and RXR antagonists. Consistently, suppression of JNK by t-RA was not affected by overexpression of either the dominant-negative RAR
or the dominant-negative RXR. These data elucidated that the antiapoptotic effect of t-RA is mediated by both nuclear
receptor-dependent and -independent mechanisms.
Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor
in the Suppression of Apoptosis by All-trans-retinoic
Acid*
*
This work was supported in part by grants from the Wellcome
Trust and the National Kidney Research Fund (to M. K.).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.
To whom correspondence should be addressed: Renal Bioengineering
Unit, Dept. of Medicine, Royal Free and University College Medical
School, University College London, Jules Thorn Inst., 7th Floor,
Middlesex Hospital, Motimer St., London W1T 3AA, UK. Tel.:
44-20-7679-9623; Fax: 44-20-7636-9941; E-mail:
m.kitamura@ucl.ac.uk.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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