TY - JOUR
T1 - Closed head injury induces upregulation of beclin 1 at the cortical site of injury
AU - Diskin, Tal
AU - Tal-Or, Pazit
AU - Erlich, Shlomit
AU - Mizrachy, Liat
AU - Alexandrovich, Alexander
AU - Shohami, Esther
AU - Pinkas-Kramarski, Ronit
PY - 2005/7
Y1 - 2005/7
N2 - 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.
AB - 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.
KW - Astrocytes
KW - Autophagy
KW - Beclin 1
KW - Brain
KW - Neurons
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=22244491605&partnerID=8YFLogxK
U2 - 10.1089/neu.2005.22.750
DO - 10.1089/neu.2005.22.750
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C2 - 16004578
AN - SCOPUS:22244491605
SN - 0897-7151
VL - 22
SP - 750
EP - 762
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
IS - 7
ER -