AJP - Renal Physiology, Vol 260, Issue 4 479-F485, Copyright © 1991 by American Physiological Society
Transient ischemia or heat stress induces a cytoprotectant protein in rat kidney
A. Emami, J. H. Schwartz and S. C. Borkan
Department of Medicine, Boston City Hospital, Boston University School of Medicine, Massachusetts 02118.
Sublethal heat exposure induces the production of heat stress protein (HSP)
72 kDa, a reported cytoprotectant, in several tissues including the rat
kidney. However, the localization and time course of HSP 72 accumulation in
the kidney in response to heat or other cell stresses such as transient
ischemia have not been described. In anesthetized rats exposed to either 42
+/- 0.5 degrees C (heat stress) or 37 degrees C (sham) for 15 min,
accumulation of HSP 72 in kidney homogenates, detected by immunoblot
analysis using a specific monoclonal anti-HSP 72 antibody, peaked 4-6 h
after heat stress and persisted for 10 days. HSP 72 appeared rapidly in
renal papilla within 1 h and in medulla and cortex within 4 h after heat
stress. No HSP 72 was detected in tissues from sham heat stress. HSP 72 was
also detected within 3 h of at least 15 min of renal ischemia in situ.
Accumulation was maximal after 60 min of ischemia and persisted for 5 days,
whereas no HSP 72 was detected after 90 min of ischemia or in the
contralateral nonischemic kidney at any time point. This study demonstrates
that transient ischemia, like heat stress, results in the rapid cytosolic
accumulation of HSP 72, a known cytoprotectant that may be important in
mediating cell repair or increasing resistance to subsequent injury.
