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J. Biol. Chem., Vol. 277, Issue 13, 11392-11400, March 29, 2002
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From the Glucose (Glc) metabolism protects cells against
oxidant injury. By virtue of their central position in both Glc uptake
and utilization, hexokinases (HKs) are ideally suited to contribute to
these effects. Compatible with this hypothesis, endogenous HK activity
correlates inversely with injury susceptibility in individual renal
cell types. We recently reported that ectopic HK expression mimics the
anti-apoptotic effects of growth factors in cultured fibroblasts, but
anti-apoptotic roles for HKs have not been examined in other cell types
or in a cellular injury model. We therefore evaluated HK overexpression
for the ability to mitigate acute oxidant-induced cell death in an
established epithelial cell culture injury model. In parallel, we
examined salutary heparin-binding epidermal growth factor (EGF)-like
growth factor (HB-EGF) treatment for the ability to 1) increase
endogenous HK activity and 2) mimic the protective effects of ectopic
HK expression. Both HK overexpression and HB-EGF increased
Glc-phosphorylating capacity and metabolism, and these changes were
associated with markedly reduced susceptibility to acute
oxidant-induced apoptosis. The uniform Glc dependence of these effects
suggests an important adaptive role for Glc metabolism, and for HK
activity in particular, in the promotion of epithelial cell survival.
These findings also support the contention that HKs contribute to the
protective effects of growth factors.
Increased Hexokinase Activity, of Either Ectopic or Endogenous
Origin, Protects Renal Epithelial Cells against Acute
Oxidant-induced Cell Death*
§,§,§
**
Department of Medicine, Section of
Nephrology, Department of Physiology & Biophysics, and
¶ Department of Molecular Genetics, College of Medicine,
University of Illinois, Chicago and § Veterans Affairs
Chicago Health Care System, West Side Division, Chicago, Illinois
60612
*
This work was supported by grants-in-aid from the National
Kidney Foundation of Illinois (to R. B. R.) and the American Heart Association of Metropolitan Chicago (to R. B. R.), as well as by a
United States Department of Veterans Affairs Merit Review Award (to
R. B. R.) and National Institutes of Health Grant AG-16927 (to
N. H.). Portions of this work were presented in preliminary form at
the 6th Annual AstraZeneca Cardiovascular Young Investigators' Forum,
August 19, 2000, in Quebec City, Quebec, Canada and at the 33rd Annual
Meeting of the American Society of Nephrology, October 14, 2000, in
Toronto, Ontario, Canada.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.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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