ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Bax Contributes to Retinal Ganglion Cell Dendritic Degeneration During Glaucoma.Molecular neurobiology · 2022Article
- Membrane Depolarization Inhibits BIMMolecular neurobiology · 2021Article
- The intrinsic apoptotic pathway lies upstream of oxidative stress in multiple organs.Free radical biology & medicine · 2020Article
- Loss of AKAP1 triggers Drp1 dephosphorylation-mediated mitochondrial fission and loss in retinal ganglion cells.Cell death & disease · 2020Article
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- Synergistic Effects of Bortezomib-OV Therapy and Anti-Invasive Strategies in Glioblastoma: A Mathematical Model.Cancers · 2019Article
- The Anti-Inflammatory Effect of Feiyangchangweiyan Capsule and Its Main Components on Pelvic Inflammatory Disease in Rats via the Regulation of the NF-Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis.Frontiers in aging neuroscience · 2019Article
- Beneficial Impact and Molecular Mechanism ofInternational journal of molecular sciences · 2018Article
- Dissociation of JNK Activation from Elevated Levels of Reactive Oxygen Species, Cytochrome c Release, and Cell Death in NGF-Deprived Sympathetic Neurons.Molecular neurobiology · 2018Article
- N-Adamantyl-4-Methylthiazol-2-Amine Attenuates Glutamate-Induced Oxidative Stress and Inflammation in the Brain.Neurotoxicity research · 2017Article
- Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration.Scientific reports · 2016Article
- Targeting TRPM2 Channels Impairs Radiation-Induced Cell Cycle Arrest and Fosters Cell Death of T Cell Leukemia Cells in a Bcl-2-Dependent Manner.Oxidative medicine and cellular longevity · 2016Article
- Bax and caspases regulate increased production of mitochondria-derived reactive species in neuronal apoptosis: LACK of A role for depletion of cytochrome c from the mitochondrial electron transport chain.Biochemistry and biophysics reports · 2015Article
- Reactive oxygen species are involved in BMP-induced dendritic growth in cultured rat sympathetic neurons.Molecular and cellular neurosciences · 2015Article
- Ceramide-induced apoptosis in renal tubular cells: a role of mitochondria and sphingosine-1-phoshate.International journal of molecular sciences · 2015Review
- Article
- GM1 ganglioside activates ERK1/2 and Akt downstream of Trk tyrosine kinase and protects PC12 cells against hydrogen peroxide toxicity.Neurochemical research · 2014Article
- Mitochondria-derived reactive oxygen species mediate caspase-dependent and -independent neuronal deaths.Molecular and cellular neurosciences · 2014Article
- In vivo antioxidative and neuroprotective effect of 4-Allyl-2-methoxyphenol against chlorpyrifos-induced neurotoxicity in rat brain.Molecular and cellular biochemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
A Bax- and, apparently, mitochondria-dependent increase in superoxide (O(2)(·-)) and other reactive oxygen species (ROS) occurs in apoptotic superior cervical ganglion (SCG) and cerebellar granule (CG) neurons. Here we show that Bax also lies upstream of ROS produced in nonapoptotic neurons and present evidence that caspases partially mediate the pro-oxidant effect of Bax. We used the O(2)(·-)-sensitive dye MitoSOX to monitor O(2)(·-) in neurons expressing different levels of Bax and mitochondrial superoxide dismutase (SOD2). Basal and apoptotic O(2)(·-) levels in both SCG and CG neurons were reduced in SOD2 wild-type (WT) cells having lower Bax concentrations. Apoptotic and nonapoptotic neurons from Bax-WT/SOD2-null but not Bax-null/SOD2-null mice had increased O(2)(·-) levels. A caspase inhibitor inhibited O(2)(·-) in both apoptotic and nonapoptotic SCG neurons. O(2)(·-) production increased when WT, but not Bax-null, SCG neurons were permeabilized and treated with active caspase 3. There was no apoptosis and little increase in O(2)(·-) in SCG neurons from caspase 3-null mice exposed to an apoptotic stimulus. O(2)(·-) levels in nonapoptotic caspase 3-null SCG neurons were lower than in WT cells but not as low as in caspase inhibitor-treated cells. These data indicate that Bax lies upstream of most O(2)(·-) produced in neurons, that caspase 3 is required for increased O(2)(·-) production during neuronal apoptosis, that caspase 3 is partially involved in O(2)(·-) production in nonapoptotic neurons, and that other caspases may also be involved in Bax-dependent O(2)(·-) production in nonapoptotic cells.
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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.