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5 INTRODUCTION: We and others have previously shown  that the stress protein HSP72 protected against focal cerebral ischemia  and excitotoxin exposure when overexpression occurred prior to the  insult, provided the extent of transgene expression was sufficiently  high, and the insult not too severe. Whether HSP72 overexpression is  protective after focal ischemia or in other brain ischemia models is  unknown. We studied whether HSP72 protected when delivered after a  stroke, and also if it protected CA1 cells against global cerebral  ischemia by using amplicon based viral vectors that permit high levels  of transgene expression.METHODS: Bipromoter, defective  herpes simplex vectors expressing HSP72 and β-galactosidase as a  reporter (or β-galactosidase only as a control) were delivered to the  striata of 21 rats 20min after 1h MCA occlusion. 48h after reperfusion,  the number of remaining reporter gene positive neurons were counted and  expressed as ratio of the number of surviving cells between ischemic to  nonischemic hemispheres. 15 h prior to the onset of global  cerebral ischemia (bilateral common carotid artery occlusion plus  hypotension; n=9), similar vectors were injected into each CA1  hippocampal subsector. Reporter gene positive cells in CA1 were counted  and compared to counts in sham operated rats injected with vector  (n=4).RESULTS: Survival among HSP72 treated groups was  significantly higher for both experiments. After post insult delivery  in the MCA occlusion model, 54.7±8.6% of HSP72 treated cells remained  versus 31.2±5.1% of control vector treated (P&lt;0.03). Following  global cerebral ischemia, 31±8% of HSP72 treated CA1 neurons remained  compared to 10±4% among controls (P&lt;0.05).CONCLUSIONS: To our knowledge, this is the first study to show that postischemic  HSP72 overexpression is protective, and that HSP72 protects CA1 neurons  from global cerebral ischemia. This suggests that this stress protein  may be a useful therapeutic target because it protects against a  variety of insults and is also effective when treatment is  delayed.

Viral vector mediated Hsp72 overexpression protects against global cerebral ischemia and when given after experimental stroke