Stress protein inductions after brain ischemia

K. Abe, J. Kawagoe, M. Aoki, K. Kogure, Y. Itoyama

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

1. Hippocampal CA1 neurons are the most vulnerable to transient cerebral ischemia. However, the mechanism has not been fully understood. 2. The mRNAs for 72-kd (HSP72) and 73-kd (HSC73) heat shock proteins (HSPs), which are located mainly in the cytoplasm, were greatly induced together in CA1 cells, with a peak at 1-2 days in gerbils. However, immunoreactive HSP72 protein was only minimally expressed in CA1 neurons. 3. The mRNA for mitochondrial HSP60 began to increase at 3 hr in CA1 cells and was sustained until 1 day. 4. The level of mRNA for cytochrome c oxidase subunit I (COX-I) progressively decreased in CA1 neurons after a transient ischemia and completely disappeared at 7 days. The activity of cytochrome c oxidase (COX) protein also showed an early decrease in CA1 cells and was followed by a reduction in the level of COX-I DNA after 2 days. 5. These results suggest that HSP gene inductions were inhibited at the translational level but that mitochondrial DNA expression was disturbed at the transcriptional level. A disturbance of mitochondrial DNA expression could cause progressive failure of energy production of CA1 cells that eventually results in neuronal cell death.

Original languageEnglish
Pages (from-to)709-719
Number of pages11
JournalCellular and molecular neurobiology
Volume18
Issue number6
DOIs
Publication statusPublished - 1998

Keywords

  • Cytochrome c oxidase
  • HSC73
  • HSP60
  • HSP72
  • Ischemia

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

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