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J. Biol. Chem., Vol. 276, Issue 15, 11870-11876, April 13, 2001
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From MAPK activities, including JNK, p38, and
ERK, are markedly enhanced after ischemia in vivo
and chemical anoxia in vitro. The relative extent of
JNK, p38, or ERK activation has been proposed to determine cell
fate after injury. A mouse model was established in which prior
exposure to ischemia protected against a second ischemic insult imposed
8 or 15 days later. In contrast to what was observed after 30 min of
bilateral ischemia, when a second period of ischemia of 30- or 35-min
duration was imposed 8 days later, there was no subsequent increase in
plasma creatinine, decrease in glomerular filtration rate, or increase
in fractional excretion of sodium. A shorter period of prior ischemia
(15 min) was partially protective against subsequent ischemic injury 8 days later. Unilateral ischemia was also protective against a subsequent ischemic insult to the same kidney, revealing that systemic
uremia is not necessary for protection. The ischemia-related activation
of JNK and p38 and outer medullary vascular congestion were
markedly mitigated by prior exposure to ischemia, whereas preconditioning had no effect on post-ischemic activation of ERK1/2. The phosphorylation of MKK7, MKK4, and MKK3/6, upstream activators of
JNK and p38, was markedly reduced by ischemic preconditioning, whereas
the post-ischemic phosphorylation of MEK1/2, the upstream activator of
ERK1/2, was unaffected by preconditioning. Pre- and post-ischemic
HSP-25 levels were much higher in the preconditioned kidney. In
summary, post-ischemic JNK and p38 (but not ERK1/2) activation was
markedly reduced in a model of kidney ischemic preconditioning that was
established in the mouse. The reduction in JNK and p38 activation can
be accounted for by reduced activation of upstream MAPK kinases. The
post-ischemic activation patterns of MAPKs may explain the remarkable
protection against ischemic injury observed in this model.
Prevention of Kidney Ischemia/Reperfusion-induced Functional
Injury and JNK, p38, and MAPK Kinase Activation by Remote Ischemic
Pretreatment*
¶,¶, and§
Medical Services, Massachusetts General
Hospital, Charlestown, Massachusetts 02129-2060, the Department of
Medicine, Harvard Medical School, Boston, Massachusetts 02114, and
§ Harvard-Massachusetts Institute of Technology Division of
Health Sciences and Technology, Boston, Massachusetts 02115-6092 and Cambridge, Massachusetts 02139-4307
*
This work was supported by National Institutes of Health
Merit Awards DK39773, DK38452, and NS10828 (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: Massachusetts
General Hospital East, Suite 4002, 149 13th St., Charlestown, MA 02129-2060. Tel.: 617-726-3770; Fax: 617-726-4356; E-mail:
joseph_bonventre@hms.harvard.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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