Differential expression of heat shock proteins 70-1 and 70-2 mRNA after ischemia-reperfusion iniury of rat kidney

Ischemia-reperfusion injury in the kidney is known to cause induction of th e inducible form of the 70 kDa heat shock protein HSP70i (or HSP72). Howeve r, knowledge of the expressional regulation of the two coding genes for HSP 70i - HSP70-1 gene and HSP70-2 gene - is very limited. We investigated the time course of HSP70-1 and -2 mRNA expression and its relation to cellular ATP levels in the renal cortex after different periods of unilateral warm r enal ischemia (10-60 min) and reperfusion (up to 60 min) in 10-week-old mal e Wistar rats. Immediately after ischemia there was a significant induction of both HSP70i genes, While HSP70-1 expression constantly increased (up to 4-fold) during reperfusion, even to a higher extent with prolongation of i schemia, HSP70-2 mRNA - which was generally expressed at a far lower level than HSP70-1 mRNA - was strongly induced (3-fold) during reperfusion only a fter brief periods (10 min) of ischemia. Cellular ATP levels rapidly droppe d to 5% with ischemia and the pattern of recovery during reperfusion signif icantly depended on the duration of the ischemic period, thus showing a goo d relation with the heat shock (protein) gene expression. We conclude that HSP70-2 is the more sensitive gene with a lower activation threshold by mil d injury, while the HSP70-1 gene mediates the major response of heat shock protein induction after severe injury.