期刊
AUTOPHAGY
卷 4, 期 1, 页码 88-90出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.5173
关键词
autophagosome; controlled cortical impact; antioxidant; head injury; LC3; mitophagy
类别
资金
- NINDS NIH HHS [P50 NS30318, R01 NS38620] Funding Source: Medline
- PHS HHS [AHA 0535365N] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038620, P50NS030318] Funding Source: NIH RePORTER
Autophagy is a homeostatic process for recycling of proteins and organelles, that increases during times of nutrient deprivation and is regulated by reactive oxygen species. We reported that autophagy can also be induced after traumatic brain injury (TBI) in mice.1 Specifically, autophagosomes and multilamellar bodies were frequently observed in cell processes and axons in injured brain regions by electron microscopy, and lipidated microtubule-associated protein light chain 3 (LC3-II), was increased after TBI vs. controls. To determine if antioxidants could reduce autophagy, separate mice were treated with the antioxidant gamma-glutamylcysteinyl ethyl ester (GCEE). Treatment with GCEE preserved total antioxidant reserves, reduced LC3-II in injured brains, and improved both behavioral and histological outcome after TBI. Here we report that LC3-II and autophagosomes were detectable in brain tissue from humans after TBI. Taken together, we show that autophagy occurs after both experimental and clinical TBI, and that oxidative stress contributes to overall neuropathology after TBI in mice, at least in part by initiating or influencing autophagy. Addendum to: Lai Y, Hickey RW, Chen Y, Bayir H, Sullivan M, Chu CT, Kochanek PM, Dixon CE, Jenkins LW, Graham SH, Watkins SC, Clark RSB. Autophagy is increased after traumatic brain injury in mice and is partially inhibited by the antioxidant gamma-glutamylcysteinyl ethyl ester. J Cereb Blood Flow Metab 2007; In press.
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