Closed head injury induces upregulation of beclin 1 at the cortical site of injury

Tal Diskin, Pazit Tal-Or, Shlomit Erlich, Liat Mizrachy, Alexander Alexandrovich, Esther Shohami, Ronit Pinkas-Kramarski*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

163 Scopus citations

Abstract

Autophagy, a bulk degradation of subcellular constituents, is activated in several neurodegenerative conditions. Beclin 1, a Bcl2 interacting protein, was found to promote autophagy. The closed head injury model was used to investigate the possible role of autophagy and Beclin 1 after traumatic brain injury. It is demonstrated that levels of Beclin-1 are dramatically increased near the site of injury. Neurons constitute the major population of cells, with the highest Beclin 1 levels near the site of injury at early stages post injury. Elevated levels of Beclin 1 protein in neurons last for at least 3 weeks. In addition, Beclin-1 expression after injury is elevated also in astrocytes starting at 3 days after injury. Confocal microscopy analysis suggests that the high levels of Beclin 1 protein in astrocytes is confined to subcellular organelles, probably lysosomes or autophagosomes. Double staining of Beclin 1 and TUNEL indicate that most of the injured cells that exhibit double staining are neurons and not astrocytes. These findings show that Beclin 1 may play a role in brain responses to head trauma. Overexpression of Beclin 1 may be important for autophagy at the lesion site and may serve as a mechanism to discard injured cells and reduce damage to cells by disposing of injured components.

Original languageEnglish
Pages (from-to)750-762
Number of pages13
JournalJournal of Neurotrauma
Volume22
Issue number7
DOIs
StatePublished - Jul 2005

Keywords

  • Astrocytes
  • Autophagy
  • Beclin 1
  • Brain
  • Neurons
  • Traumatic brain injury

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