ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Mitochondrial depolarization is not required for neuronal apoptosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The trial behind it
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Who cites it
39 citing papers in PubMed, 181 citations in OpenAlex.
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- Combined Treatment with Cryptocaryone and Ultraviolet C Promotes Antiproliferation and Apoptosis of Oral Cancer Cells.International journal of molecular sciences · 2022Article
- Disease-specific phenotypes in iPSC-derived neural stem cells with POLG mutations.EMBO molecular medicine · 2020Article
- Apoptotic cell death regulation in neurons.The FEBS journal · 2019Review
- In Vitro Anti-proliferative Activity and Mechanism of Action ofInternational journal of molecular sciences · 2019Article
- CSPGs inhibit axon branching by impairing mitochondria-dependent regulation of actin dynamics and axonal translation.Developmental neurobiology · 2017Article
- Oxidative stress response in neural stem cells exposed to different superparamagnetic iron oxide nanoparticles.International journal of nanomedicine · 2016Article
- Re-engineered p53 activates apoptosis in vivo and causes primary tumor regression in a dominant negative breast cancer xenograft model.Gene therapy · 2014Article
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- Latrepirdine is a potent activator of AMP-activated protein kinase and reduces neuronal excitability.Translational psychiatry · 2013Article
- The DNA binding domain of p53 is sufficient to trigger a potent apoptotic response at the mitochondria.Molecular pharmaceutics · 2013Article
- Double strand breaks and cell-cycle arrest induced by the cyanobacterial toxin cylindrospermopsin in HepG2 cells.Marine drugs · 2013Article
- Effects of transmembrane potential and pH gradient on the cytochrome c-promoted fusion of mitochondrial mimetic membranes.Journal of bioenergetics and biomembranes · 2013Article
- Involvement of dynamin-related protein 1 in free fatty acid-induced INS-1-derived cell apoptosis.PloS one · 2012Article
- Autophagy protects against aminochrome-induced cell death in substantia nigra-derived cell line.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Mitochondrial membrane potential probes and the proton gradient: a practical usage guide.BioTechniques · 2011Review
- Chloroquine activates the p53 pathway and induces apoptosis in human glioma cells.Neuro-oncology · 2010Article
- Bcl-2 family proteins as regulators of oxidative stress.Seminars in cancer biology · 2009Review
- Caspase-independent apoptosis in Friend's erythroleukemia cells: role of mitochondrial ATP synthesis impairment in relocation of apoptosis-inducing factor and endonuclease G.Journal of bioenergetics and biomembranes · 2009Article
- Mitochondrial-targeted active Akt protects SH-SY5Y neuroblastoma cells from staurosporine-induced apoptotic cell death.Journal of cellular biochemistry · 2007Article
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
Mitochondria are sites of cellular energy production but may also influence life and death decisions by initiating or inhibiting cell death. Mitochondrial depolarization and the subsequent release of pro-apoptotic factors have been suggested to be required for the activation of a cell death program in some forms of neuronal apoptosis. We induced apoptosis in cultured rat hippocampal neurons by exposure to the protein kinase inhibitor staurosporine (STS) (300 nM). The time course of mitochondrial membrane potential (DeltaPsi(m)) during apoptosis was examined using the probe tetramethylrhodamine ethyl ester (TMRE). Cells exhibited no decrease in TMRE fluorescence, indicative of mitochondrial depolarization, up to 8 hr after STS exposure. Rather, baseline TMRE fluorescence remained unchanged up to 2 hr and thereafter actually increased significantly. Throughout this time period, the mitochondria could also be depolarized with the protonophore carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP, 0.1 microM), exhibiting the same relative magnitude of fluorescence release (unquenching) as controls. Even after 16 hr of staurosporine treatment, neurons that showed signs of nuclear apoptosis maintained DeltaPsi(m) and could be depolarized with FCCP. In contrast, caspase-3-like activity had increased roughly sevenfold by 2 hr and >20-fold by 8 hr. Double-labeling of hippocampal neurons with the potential-sensitive probe Mitotracker Red Chloromethyl X-Rosamine and an antibody to cytochrome c demonstrated at the subcellular level that mitochondrial cytochrome c release also occurred in the absence of mitochondrial depolarization. These data suggest that mitochondrial depolarization is not a decisive event in neuronal apoptosis.
Indexed as
Identifiers
10460246PMC6782497W1514719303What OpenQuestion holds
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.