Effects of global cerebral ischemia and preconditioning on heat shock protein 27 immunocontent and phosphorylation in rat hippocampus

Global cerebral ischemia, with or without preconditioning, leads to an incr ease in heat shock protein 27 (HSP27) immunocontent and alterations in HSP2 7 phosphorylation in CA1 and dentate gyrus areas of the hippocampus. We stu died different times of reperfusion (1. 4, 7, 14, 21 and 30 days) using 2 m in, 10 min or 2+ 10 min of ischemia. The results showed an increase in HSP2 7 immunocontent of about 300% after 10 min of ischemia in CA1 and dentate g yrus. CA1 a hippocampal vulnerable area, showed an increase in HSP27 phosph orylation, parallel with immunocontent. In dentate gyrus. a resistant area, the increase in HSP phosphorylation was lower than immunocontent. After pr econditioned ischemia (2+10 min), when CA1 neurons are protected to a letha l, 10 min insult, we observed an increase in HSP immunocontent and a decrea se in phosphorylation in both regions of the hippocampus, suggesting that, when there is no neuronal death, HSP27 in a vulnerable area responds simila rly to the resistant area. When dephosphorylated. HSP27 acts as a chaperone, protecting other proteins from denaturation. As it is markedly expressed in astrocytes, we suggest t hat HSP27 could be protecting hippocampal astrocytes, which Could then be h elping neurons to resist to the insult, maintaining tissue normal homeostas is. (C) 2001 IBRO, published by Elsevier Science Ltd. All rights reserved.