GluR3B Ab’s induced oligodendrocyte precursor cells excitotoxicity via mitochondrial dysfunction

Highlights • GluR3B Ab’s induces apoptotic cell death in primary rat OPCs via AMPAR activation. • AMPAR activation causes intracellular Ca2+ overload and mitochondrial membrane damage. • Mitochondrial dysfunction is involved in OPCs apoptosis induced by GluR3B Ab’s.

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Bibliographic Details
Published in:Brain research bulletin 2017-04, Vol.130, p.60-66
Main Authors: Liu, Yi, Chen, Yan, Du, Wan Tong, Wu, Xiu Xiang, Dong, Fu Xing, Qu, Xue Bin, Fan, Hong Bin, Yao, Rui Qin
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Autoantibodies
Calcium - metabolism
Cell Survival
Cells, Cultured
Excitotoxicity
Glutamate receptor antibody
Mitochondria
Mitochondria - immunology
Mitochondria - metabolism
Neurology
Oligodendrocyte precursor cells
Oligodendrocyte Precursor Cells - immunology
Oligodendrocyte Precursor Cells - physiology
Rats, Sprague-Dawley
Reactive Oxygen Species
Receptors, AMPA - immunology
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Summary:Highlights • GluR3B Ab’s induces apoptotic cell death in primary rat OPCs via AMPAR activation. • AMPAR activation causes intracellular Ca2+ overload and mitochondrial membrane damage. • Mitochondrial dysfunction is involved in OPCs apoptosis induced by GluR3B Ab’s.
ISSN:0361-9230
1873-2747
DOI:10.1016/j.brainresbull.2016.12.016