ArticleAntioxidants & redox signaling2015
Bcl-xL is necessary for neurite outgrowth in hippocampal neurons.
Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Erythropoietin for the prevention of postoperative neurocognitive disorder in older adult patients undergoing total joint arthroplasty: a randomized controlled study.BMC anesthesiology · 2024Trial
- Bedaquiline inhibits the ATP synthase leak channel and prevents glutamate-induced neuronal death.Biophysical reports · 2026Article
- BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Bedaquiline inhibits the ATP synthase leak channel and prevents glutamate-induced neuronal death.bioRxiv : the preprint server for biology · 2026Article
- Synaptamide regulates astroglial functional activity after cerebral cortex injury.Inflammopharmacology · 2025Article
- GSK-126 Attenuates Cell Apoptosis in Ischemic Brain Injury by Modulating the EZH2-H3K27me3-Bcl2l1 Axis.Molecular neurobiology · 2024Article
- Tumorigenicity decrease in Bcl-xL deficient MDCK cells ensuring the safety for influenza vaccine production.PloS one · 2024Article
- Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL.Nutrition research (New York, N.Y.) · 2022Article
- Erythropoietin regulates signaling pathways associated with neuroprotective events.Experimental brain research · 2022Review
- Paeoniflorin ameliorates ischemic injury in rat brain via inhibiting cytochrome c/caspase3/HDAC4 pathway.Acta pharmacologica Sinica · 2022Article
- Neuroglial Senescence, α-Synucleinopathy, and the Therapeutic Potential of Senolytics in Parkinson's Disease.Frontiers in neuroscience · 2022Review
- Bcl-xL Is Required by Primary Hippocampal Neurons during Development to Support Local Energy Metabolism at Neurites.Biology · 2021Article
- Anthocyanins Promote Learning through Modulation of Synaptic Plasticity Related Proteins in an Animal Model of Ageing.Antioxidants (Basel, Switzerland) · 2021Article
- Involvement of Bcl-xL in Neuronal Function and Development.International journal of molecular sciences · 2021Review
- Constraint-induced movement therapy enhances AMPA receptor-dependent synaptic plasticity in the ipsilateral hemisphere following ischemic stroke.Neural regeneration research · 2021Article
- Oxidative stress battles neuronal Bcl-xL in a fight to the death.Neural regeneration research · 2021Article
- Development of Conformational Antibodies to Detect Bcl-xL's Amyloid Aggregates in Metal-Induced Apoptotic Neuroblastoma Cells.International journal of molecular sciences · 2020Article
- Anti-Apoptotic Effects of Carotenoids in Neurodegeneration.Molecules (Basel, Switzerland) · 2020Review
- Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons.International journal of molecular sciences · 2019Article
- Parkinson's disease protein DJ-1 regulates ATP synthase protein components to increase neuronal process outgrowth.Cell death & disease · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
aimsB-cell lymphoma-extra large (Bcl-xL) protects survival in dividing cells and developing neurons, but was not known to regulate growth. Growth and synapse formation are indispensable for neuronal survival in development, inextricably linking these processes. We have previously shown that, during synaptic plasticity, Bcl-xL produces changes in synapse number, size, activity, and mitochondrial metabolism. In this study, we determine whether Bcl-xL is required for healthy neurite outgrowth and whether neurite outgrowth is necessary for survival in developing neurons in the presence or absence of stress.
resultsDepletion of endogenous Bcl-xL impairs neurite outgrowth in hippocampal neurons followed by delayed cell death which is dependent on upregulation of death receptor 6 (DR6), a molecule that regulates axonal pruning. Under hypoxic conditions, Bcl-xL-depleted neurons demonstrate increased vulnerability to neuronal process loss and to death compared with hypoxic controls. Endogenous DR6 expression and upregulation during hypoxia are associated with worsened neurite damage; depletion of DR6 partially rescues neuronal process loss, placing DR6 downstream of the effects of Bcl-xL on neuronal process outgrowth and protection. In vivo ischemia produces early increases in DR6, suggesting a role for DR6 in brain injury. INNOVATION: We suggest that DR6 levels are usually suppressed by Bcl-xL; Bcl-xL depletion leads to upregulation of DR6, failure of neuronal outgrowth in nonstressed cells, and exacerbation of hypoxia-induced neuronal injury.
conclusionBcl-xL regulates neuronal outgrowth during development and protects neurites from hypoxic insult, as opposed by DR6. Factors that enhance neurite formation may protect neurons against hypoxic injury or neurodegenerative stimuli.
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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.