1. Neuroglobin protects PC12 cells against β-amyloid-induced cell injury
- Author
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Richard C. Li, Farzan Pouranfar, Yang Wang, David Gozal, Matthew W. Morris, and Seung Kwan Lee
- Subjects
Aging ,Amyloid ,Amyloid beta ,Neuroglobin ,Apoptosis ,Nerve Tissue Proteins ,medicine.disease_cause ,PC12 Cells ,Neuroprotection ,Article ,medicine ,Animals ,Neurons ,chemistry.chemical_classification ,Reactive oxygen species ,Amyloid beta-Peptides ,biology ,General Neuroscience ,Peptide Fragments ,Globins ,Rats ,Cell biology ,Oxidative Stress ,Neuroprotective Agents ,chemistry ,biology.protein ,Neurology (clinical) ,Geriatrics and Gerontology ,Reactive Oxygen Species ,Oxidative stress ,Intracellular ,Developmental Biology - Abstract
Excessive accumulation of amyloid beta (Abeta) has been proposed as a pivotal event in the pathogenesis of Alzheimer's disease. Possible mechanisms underlying Abeta-induced neuronal cytotoxicity include excess production of reactive oxidative species (ROS) and apoptosis. Neuroglobin (Ngb), a newly discovered globin in vertebrates that exhibits neuroprotective functions, may have a potential role in scavenging ROS. To examine the potential protective role of Ngb in Abeta-induced cytotoxicity, PC12 cells were treated with Abeta (1-42 fragment) for 24h. Abeta treatments increased ROS production in PC12 cells. Overexpression of Ngb but not Ngb mutant in the PC12 cells significantly attenuated Abeta-induced ROS production and lipids peroxidation. Furthermore, overexpression of Ngb also attenuated Abeta-induced mitochondrial dysfunction and apoptosis, and promoted cell survival in PC12 cells. Therefore, Ngb may act as an intracellular ROS scavenger, and such antioxidant properties may play a protective role against Abeta-induced cell injury.
- Published
- 2008
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