ArticleASN neuro2013
Identification of Bax-interacting proteins in oligodendrocyte progenitors during glutamate excitotoxicity and perinatal hypoxia-ischemia.
Article in ASN neuro, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Differential effects of hypothermia and memantine in neonatal hypoxia-ischemia.Metabolic brain disease · 2025Article
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Activation of glutamatergic neurons in the somatosensory cortex promotes remyelination in ischemic vascular dementia.Fundamental research · 2024Article
- Cerebral Ischemic Preconditioning Aggravates Death of Oligodendrocytes.Biomolecules · 2022Article
- GABA Receptor Agonists Protect From Excitotoxic Damage Induced by AMPA in Oligodendrocytes.Frontiers in pharmacology · 2022Article
- Chlorogenic Acid Prevents AMPA-Mediated Excitotoxicity in Optic Nerve Oligodendrocytes Through a PKC and Caspase-Dependent Pathways.Neurotoxicity research · 2018Article
- Article
- Attenuation of Glutamate-Induced Excitotoxicity by Withanolide-A in Neuron-Like Cells: Role for PI3K/Akt/MAPK Signaling Pathway.Molecular neurobiology · 2018Article
- Inhibition of Casein Kinase 2 Protects Oligodendrocytes From Excitotoxicity by Attenuating JNK/p53 Signaling Cascade.Frontiers in molecular neuroscience · 2018Article
- Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity.Cell death and differentiation · 2017Article
- Embracing oligodendrocyte diversity in the context of perinatal injury.Neural regeneration research · 2017Review
- Perinatal Brain Injury As a Consequence of Preterm Birth and Intrauterine Inflammation: Designing Targeted Stem Cell Therapies.Frontiers in neuroscience · 2017Review
- DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways.Molecular neurobiology · 2016Article
- Selected gene profiles of stressed NSC-34 cells and rat spinal cord following peripheral nerve reconstruction and minocycline treatment.Experimental and therapeutic medicine · 2016Article
- Cofilin as a Promising Therapeutic Target for Ischemic and Hemorrhagic Stroke.Translational stroke research · 2016Review
- Article
- Microarray Analysis Reveals Increased Transcriptional Repression and Reduced Metabolic Activity but Not Major Changes in the Core Apoptotic Machinery during Maturation of Sympathetic Neurons.Frontiers in cellular neuroscience · 2016Article
- The role of inflammation in perinatal brain injury.Nature reviews. Neurology · 2015Review
- Melatonin attenuates intermittent hypoxia-induced lipid peroxidation and local inflammation in rat adrenal medulla.International journal of molecular sciences · 2014Article
- Molecular features of neural stem cells enable their enrichment using pharmacological inhibitors of survival-promoting kinases.Journal of neurochemistry · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
OPC (oligodendrocyte progenitor cell) death contributes significantly to the pathology and functional deficits following hypoxic-ischemic injury in the immature brain and to deficits resulting from demyelinating diseases, trauma and degenerative disorders in the adult CNS. Glutamate toxicity is a major cause of oligodendroglial death in diverse CNS disorders, and previous studies have demonstrated that AMPA/kainate receptors require the pro-apoptotic protein Bax in OPCs undergoing apoptosis. The goal of the present study was to define the pro-apoptotic and anti-apoptotic effectors that regulate Bax in healthy OPCs and after exposure to excess glutamate in vitro and following H-I (hypoxia-ischemia) in the immature rat brain. We show that Bax associates with a truncated form of Bid, a BH3-only domain protein, subsequent to glutamate treatment. Furthermore, glutamate exposure reduces Bax association with the anti-apoptotic Bcl family member, Bcl-xL. Cell fractionation studies demonstrated that both Bax and Bid translocate from the cytoplasm to mitochondria during the early stages of cell death consistent with a role for Bid as an activator, whereas Bcl-xL, which normally complexes with both Bax and Bid, disassociates from these complexes when OPCs are exposed to excess glutamate. Bax remained unactivated in the presence of insulin-like growth factor-1, and the Bcl-xL complexes were protected. Our data similarly demonstrate loss of Bcl-xL-Bax association in white matter following H-I and implicate active Bad in Bax-mediated OPC death. To identify other Bax-binding partners, we used proteomics and identified cofilin as a Bax-associated protein in OPCs. Cofilin and Bax associated in healthy OPCs, whereas the Bax-cofilin association was disrupted during glutamate-induced OPC apoptosis.
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Registered trials
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