ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Death receptors and caspases but not mitochondria are activated in the GDNF- or BDNF-deprived dopaminergic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Genetic influence of the brain on epigenetic age acceleration: evidence of a large-scale genetic correlation study.Biogerontology · 2025Article
- BDNF/proBDNF Interplay in the Mediation of Neuronal Apoptotic Mechanisms in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Survival and Neurogenesis-Promoting Effects of the Co-Overexpression ofLife (Basel, Switzerland) · 2022Article
- CDNF Interacts with ER Chaperones and Requires UPR Sensors to Promote Neuronal Survival.International journal of molecular sciences · 2022Article
- Nurr1 Is Not an Essential Regulator of BDNF in Mouse Cortical Neurons.International journal of molecular sciences · 2022Article
- Small-Molecule Inhibitors of the RNA M6A Demethylases FTO Potently Support the Survival of Dopamine Neurons.International journal of molecular sciences · 2021Article
- FAIM-S functions as a negative regulator of NF-κB pathway and blocks cell cycle progression in NSCLC cells.Cell cycle (Georgetown, Tex.) · 2020Article
- Article
- Mitochondria: A Connecting Link in the Major Depressive Disorder Jigsaw.Current neuropharmacology · 2019Review
- Caspase-independent programmed cell death triggers CaBioscience reports · 2018Article
- Antioxidative CXXC Peptide Motif From Mesencephalic Astrocyte-Derived Neurotrophic Factor Antagonizes Programmed Cell Death.Frontiers in cell and developmental biology · 2018Article
- Transcription factor Six2 mediates the protection of GDNF on 6-OHDA lesioned dopaminergic neurons by regulating Smurf1 expression.Cell death & disease · 2016Article
- 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
- Neurodegeneration and neuroinflammation: two processes, one target.Neural regeneration research · 2015Article
- Astroglial U87 Cells Protect Neuronal SH-SY5Y Cells from Indirect Effect of Radiation by Reducing DNA Damage and Inhibiting Fas Mediated Apoptotic Pathway in Coculture System.Neurochemical research · 2015Article
- Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death.Cell death & disease · 2015Article
- Molecular mechanisms of dopaminergic subset specification: fundamental aspects and clinical perspectives.Cellular and molecular life sciences : CMLS · 2014Review
- DYRK1A promotes dopaminergic neuron survival in the developing brain and in a mouse model of Parkinson's disease.Cell death & disease · 2014Article
- Changes in mitochondrial function are pivotal in neurodegenerative and psychiatric disorders: how important is BDNF?British journal of pharmacology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotrophic factors, including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF), promote survival of midbrain dopaminergic neurons, but the death pathways activated in the dopaminergic neurons by deprivation of these factors are poorly studied. We show here that deprivation of GDNF or BDNF triggers a novel mitochondria-independent death pathway in the cultured embryonic dopaminergic neurons: cytochrome c was not released from the mitochondria to cytosol, proapoptotic protein Bax was not activated, and overexpressed Bcl-xL did not block the death. Caspases were critically required, because the death was completely blocked by caspase inhibitor BAF [boc-aspartyl(OMe)-fluoromethylketone] and overexpression of dominant-negative mutants of caspase-9, -3, and -7 significantly blocked the death. Also, the death receptor pathway was involved, because blockage of caspase-8 or FADD (Fas-associated protein with death domain), an adapter required for caspase-8 activation, inhibited death induced by GDNF or BDNF deprivation. Ligation of Fas by agonistic anti-Fas antibody induced apoptosis in the GDNF- or BDNF-maintained neurons, and inhibition of Fas by Fas-Fc chimera blocked the death of GDNF- or BDNF-deprived neurons, whereas FAIM(L) (long isoform of Fas apoptosis inhibitory molecule) could control the activity of Fas in the dopaminergic neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.