title: Closed head injury induces upregulation of Beclin 1 at the cortical site of injury.
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.
authors: Department of Neurobiochemistry, Tel-Aviv University, Ramat-Aviv, Israel.
authors: Tal
authors: T
authors: Diskin
authors: Pazit
authors: P
authors: Tal-Or
authors: Shlomit
authors: S
authors: Erlich
authors: Liat
authors: L
authors: Mizrachy
authors: Alexander
authors: A
authors: Alexandrovich
authors: Esther
authors: E
authors: Shohami
authors: Ronit
authors: R
authors: Pinkas-Kramarski
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins; D001253:Astrocytes / Q000378:metabolism / Q000648:ultrastructure; D001343:Autophagy / Q000502:physiology*; D000071186:Beclin-1; D015415:Biomarkers; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology; D016923:Cell Death / Q000502:physiology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D016489:Head Injuries, Closed / Q000378:metabolism* / Q000503:physiopathology; D008247:Lysosomes / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009410:Nerve Degeneration / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000648:ultrastructure; D011506:Proteins / Q000378:metabolism*; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology*
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C115010:Becn1 protein, mouse; D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D011506:Proteins