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J. Biol. Chem., Vol. 277, Issue 3, 2040-2049, January 18, 2002
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From the Medical Services, Massachusetts General Hospital,
Charlestown, Massachusetts 02129, the Department of Medicine, Harvard
Medical School, Boston, Massachusetts 02114, the Harvard-Massachusetts
Institute of Technology Division of Health Sciences and Technology,
Boston, Massachusetts 02115
Protection against ischemic kidney injury is
afforded by 24 h of ureteral obstruction (UO) applied 6 or 8 days
prior to the ischemia. Uremia or humoral factors are not responsible
for the protection, since unilateral UO confers protection on that
kidney but not the contralateral kidney. Prior UO results in reduced postischemic outer medullary congestion and leukocyte infiltration. Prior UO results in reduced postischemic phosphorylation of
c-Jun N-terminal stress-activated protein kinase 1/2 (JNK1/2), p38, mitogen-activated protein kinase (MAPK) kinase 4 (MKK4), and MKK3/6. Very few cells stain positively for proliferating cell nuclear antigen after obstruction, indicating that subsequent protection against ischemia is not related to proliferation with increased numbers
of newly formed daughter cells more resistant to injury. UO increases
the expression of heat shock protein (HSP)-25 and HSP-72. The increased
HSP-25 expression persists for 6 or 8 days, whereas HSP-72 does not.
HSP-25 expression is increased in the proximal tubule cells in the
outer stripe of the outer medulla postobstruction, prior to, and
24 h after ischemia. In LLC-PK1 renal epithelial
cells, adenovirus-expressed human HSP-27 confers resistance to
chemical anoxia and oxidative stress. Increased HSP-27 expression in
LLC-PK1 cells results in reduced
H2O2-induced phosphorylation of JNK1/2 and
p38. In conclusion, prior transient UO renders the kidney
resistant to ischemia. This resistance to functional consequences of
ischemia is associated with reduced postischemic activation of JNK, p38
MAP kinases, and their upstream MAPK kinases. The persistent increase
in HSP-25 that occurs as a result of UO may contribute to the reduction
in phosphorylation of MAPKs that have been implicated in adhesion
molecule up-regulation and cell death.
Prevention of Kidney Ischemia/Reperfusion-induced
Functional Injury, MAPK and MAPK Kinase Activation, and Inflammation by
Remote Transient Ureteral Obstruction*
*
This work was supported by National Institutes of Health
MERIT Awards DK 39773, DK 38452, and NS 10828 (to J. V. B.).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: Suite 4002, Massachusetts General Hospital East, 149 13th St., Charlestown, MA 02129. Tel.: 617-726-3770; Fax: 617-726-4356; E-mail:
joseph_bonventre@hms.harvard.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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