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J. Biol. Chem., Vol. 275, Issue 52, 40904-40909, December 29, 2000
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From the Department of Medicine, Division of Nephrology,
Hypertension and Transplantation, Department of Pediatrics, Department
of Neuroscience, University of Florida,
Gainesville, Florida 32610
Heme oxygenase-1 (HO-1), a 32-kDa microsomal
enzyme, is induced as a beneficial and adaptive response in
cells/tissues exposed to oxidative stress. Transforming growth
factor-
Smad7-dependent Regulation of Heme Oxygenase-1 by
Transforming Growth Factor-
in Human Renal Epithelial Cells*
,
1 (TGF-1) is a regulatory cytokine that has been
implicated in a variety of renal diseases where it promotes
extracellular matrix deposition and proinflammatory events. We
hypothesize that the release of TGF-1 via autocrine and/or paracrine
pathways may induce HO-1 and serve as a protective response in renal
injury. To understand the molecular mechanism of HO-1 induction by
TGF-1, we exposed confluent human renal proximal tubule cells to
TGF-1 and observed a significant induction of HO-1 mRNA at
4 h with a maximal induction at 8 h. This induction was
accompanied by increased expression of HO-1 protein. TGF-1 treatment
in conjunction with actinomycin D or cycloheximide demonstrated that
induction of HO-1 mRNA requires de novo transcription
and, in part, protein synthesis. Exposure to TGF-1 resulted in
marked induction of Smad7 mRNA with no effect on Smad6 expression.
Overexpression of Smad7, but not Smad6, inhibited TGF-1-mediated
induction of endogenous HO-1 gene expression. We speculate that the
induction of HO-1 in the kidney is an adaptive response to the
inflammatory effects of TGF-1 and manipulations of the Smad pathway
to alter HO-1 expression may serve as a potential therapeutic target.
*
This work was supported by National Institutes of Health
Grants K08 DK02446 and R03 DK56279 (to A. A.) and HL39593 (to
H. S. N.).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.
Supported by National Institutes of Health Grant T32 DK07518 (to
the Division of Nephrology, University of Florida).
§
To whom correspondence should be addressed: Division of Nephrology,
Hypertension, and Transplantation, Box 100224, JHMHC, 1600 S.W. Archer
Rd., University of Florida, Gainesville, FL 32610. Tel.: 352-392-4008;
Fax: 352-392-3581; E-mail: agarwal@nersp.nerdc.ufl.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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