THE RESPONSE OF HEAT-SHOCK PROTEINS-25 AND PROTEINS-72 TO ISCHEMIA INDIFFERENT KIDNEY ZONES

Induction of heat shock proteins (HSPs) following cell injury contribu tes to the protection of vital cell functions. It was, therefore, of i nterest to study the effects of transient renal ischaemia on the abund ance and distribution of two HSPs, HSP25 and HSP72, in renal tissue us ing Western-blot techniques, Analyses were performed on the supernatan t (HSP25, HSP72) and pellet (HSP25) of homogenates obtained from corte x (CX) and outer (OM) and inner (IM) medulla of the rat kidney immedia tely after 60 min of ischaemia followed by varying periods of reperfus ion. Ischaemia of the left kidney caused HSP25 contents to decrease in CX, OM and IM by 73, 89 and 54% respectively, compared with the corre sponding zones of the contralateral control kidney. This initial decre ase in supernatant HSP25 was accompanied by an increased abundance of HSP25 in the pellet. Following reperfusion. HSP25 contents in the supe rnatant gradually increased in CX and OM, reaching, after 24 h, values that were 5.4- and 2.5-fold higher, respectively, than those in the c ontrol kidneys. After 7 or 14 days of reperfusion, HSP25 contents had not completely normalised in CX, but had reached control levels in OM. In IM, the HSP25 content remained below control throughout the entire reperfusion period. HSP72 (supernatant) was below the detection limit in the CX of the control kidney. Similar to the level of HSP25, that of HSP72 was also markedly lower in OM and IM immediately after ischae mia. The intrarenal distribution of HSP72 and the sequence of zonal ch anges in HSP72 contents were similar to those observed for HSP25. Thes e results are compatible with the view that, during ischaemia and the initial reperfusion period, HSP25 migrates from the cytoplasmic compar tment (supernatant) into the nucleus and/or associates with cytoskelet al structures. The observation that both HSP25 and HSP72 are transient ly induced in CX and OM, but not in IM, may be explained by the fact t hat, while all kidney cells are exposed to ischaemic stress, only inne r medullary cells experience a major postischaemic attenuation of osmo tic stress.