Gene transfer of HSP72 protects cornu ammonis 1 region of the hippocampus neurons from global ischemia: Influence of Bcl‐2

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Abstract
We investigated whether HSV gene transfer of HSP72 in vivo and in vitro: (1) protected cornu ammonis 1 region of the hippocampus neurons from global cerebral ischemia; and (2) affected Bcl-2 expression. HSV vectors expressing HSP72 and β-galactosidase (reporter) or β-galactosidase only (control vector) were injected into cornu ammonis 1 region of the hippocampus 15 hours before induction of global cerebral ischemia (n = 10) and sham-operated rats (n = 8). HSP72 vector–treated rats displayed significantly more surviving transfected neurons (X-gal-positive, 31 ± 8) compared with control vector–treated rats (10 ± 4) after global cerebral ischemia. Sham-operated rats displayed similar numbers of X-gal–positive neurons (HSP72 vector 18 ± 8 vs control vector 20 ± 7). The percentage of β-galactosidase and Bcl-2 coexpressing neurons in HSP72-treated rats after global cerebral ischemia (84 ± 4%) was greater than that in control vector–treated rats (58 ± 9%). The percentage of β-galactosidase and Bcl-2 coexpressing neurons in sham-operated rats was similar in HSP72 (93 ± 7%) and in control vector–treated rats (88 ± 12%). HSP72 vector transfection led to 12 times as much Bcl-2 expression as the control vector in uninjured hippocampal neuronal cultures. In injured (oxygen-glucose deprivation) hippocampal neuron cultures, HSP72 vector transfection led to 2.8 times as much Bcl-2 expression as control vector. We show that HSP72 overexpression protects cornu ammonis 1 region of the hippocampus neurons from global cerebral ischemia, and that this protection may be mediated in part by increased Bcl-2 expression.