Premium
Defective Herpes Simplex Virus Vectors Expressing the Rat Brain Stress‐Inducible Heat Shock Protein 72 Protect Cultured Neurons from Severe Heat Shock
Author(s) -
Fink Sheri L.,
Chang Louis K.,
Ho Dora Y.,
Sapolsky Robert M.
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68030961.x
Subject(s) - heat shock protein , herpes simplex virus , biology , hippocampal formation , hsp60 , transfection , heat shock , shock (circulatory) , microbiology and biotechnology , hsp70 , gene , immunology , neuroscience , virus , medicine , biochemistry
Recently, preinduction of the heat shock response has been shown to protect CNS neurons undergoing various stressful insults, e.g., heat, ischemia, or exposure to excitotoxins. However, it is not known which of the proteins induced by the heat shock response mediate the protective effects. Previous correlative evidence points to a role for the highly stress‐induced 72‐kDa heat shock protein (hsp72). However, it is not known whether hsp72 expression alone can protect against a range of acute neuronal insults. We constructed a herpes simplex virus‐1 vector carrying the rat brain stress‐inducible hsp72 gene and the Escherichia coli lacZ (marker) gene. Infection with the vector caused hippocampal neurons to coexpress hsp72 and β‐galactosidase. Infection with a control vector led to marker gene expression only. Overexpression of hsp72 protected cultured hippocampal neurons against a heat shock but not against the metabolic toxin 3‐nitropropionic acid or the excitotoxin glutamate. This is the first published report of protection following heat shock protein transfection in CNS neurons.