Expression of vimentin increases in the hippocampus and cerebral cortex after entorhinal cortex lesioning and in response to transforming growth factor beta 1

Abstract

Entorhinal cortex lesions (ECL) that damage the perforant path to the dentate gyrus of the hippocampal formation were used to model the regulation of vimentin (VIM) mRNA. ECL increased VIM mRNA in the ipsilateral hippocampus and in the ipsilateral cortex including the wound cavity within 1 day. By in situ hybridization, at 4 days post-ECL, VIM mRNA increased two-fold in the molecular layer of the dentate gyrus. VIM protein was co-localized by immunocytochemistry to astrocytes and microglia/macrophages. Transforming growth factor-beta 1 (TGF-beta 1), which was previously shown to increase in microglia/macrophages of the molecular layer after hippocampal deafferentation by ECL, was investigated as a regulator of VIM expression. Infusions of TGF-beta 1 into the lateral ventricle induced VIM mRNA with dose-dependence, e.g. infusion of 100 ng TGF-beta 1 increased VIM mRNA three-fold. The increase in VIM mRNA was localized by in situ hybridization to astrocytes and microglia in the molecular layer of the dentate gyrus. These findings further implicate TGF-beta 1 as a regulator of cytoskeletal proteins during synaptic reorganization.