Induction of stress response proteins and experimental renal ischemia/reperfusion.
BACKGROUND: The induction of stress response (heat shock) proteins (HSPs) is a highly conserved response that protects many cell types from diverse physiological and environmental stressors. We tested the hypothesis that the induction of HSPs is protective in experimental renal ischemia/reperfusion injury. METHODS: The effect of prior heat stress was examined in a rat model of renal ischemia. Postischemic renal function, histopathology, myeloperoxidase activity, and mortality were determined in hyperthermia and sham hyperthermia groups. RESULTS: HSP84, HSP70, and HSP22 mRNA were increased after eight minutes but not four minutes of hyperthermia. The induction of HSP84 and HSP70 was blocked by pretreatment with quercetin. Improvement in renal function, mortality, and histologic abnormalities was seen with eight minutes of hyperthermia six hours before ischemia. Protection was dependent on the timing of ischemia relative to heat stress and was not observed when HSPs were not induced. Postischemic increases in renal myeloperoxidase activity were markedly attenuated in the hyperthermia compared with the sham hyperthermia group. CONCLUSION: Endogenous protective mechanisms may be important in renal ischemia/reperfusion injury.[1]References
- Induction of stress response proteins and experimental renal ischemia/reperfusion. Kelly, K.J., Baird, N.R., Greene, A.L. Kidney Int. (2001) [Pubmed]
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