GluR3B Ab's induced oligodendrocyte precursor cells excitotoxicity via mitochondrial dysfunction.

Abstract:

:Studies have indicated that glutamate receptor subunit 3 peptide B antibodies (GluR3B Ab's) by directing against a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid subtype glutamate receptors (AMPARs) subunit 3 (GluR3B) was involved in the hippocampal neuron damage in the pathogenesis of epilepsy. Glutamate accumulation is critical for oligodendrocyte precursors (OPCs) excitotoxic injury. However, remarkably little is known about whether GluR3B Ab's causes OPCs excitotoxicity, and the underlying mechanisms remain unclear. In this study, we found that the survival rate of OPCs decreased, apoptosis increased and the release of LDH increased with GluR3B Ab's treatment. GluR3B Ab's enhanced the level of intracellular Ca2+ and reactive oxygen species (ROS), caused mitochondrial potential collapse measured by JC-1 and promoted mitochondrial cytochrome C release. AMPARs antagonist NBQX reversed OPCs apoptosis caused by GluR3B Ab's. Taken together, these data suggests that AMPAR was involved in GluR3B Ab's-induced OPCs toxicity by mitochondrial dysfunction. The study revealed a new mechanism for OPCs excitotoxicity in many central nervous system diseases such as epilepsy.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Liu Y,Chen Y,Du WT,Wu XX,Dong FX,Qu XB,Fan HB,Yao RQ

doi

10.1016/j.brainresbull.2016.12.016

subject

Has Abstract

pub_date

2017-04-01 00:00:00

pages

60-66

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(16)30350-1

journal_volume

130

pub_type

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