ArticleJournal of virology2006
Role of the mitochondrial signaling pathway in murine coronavirus-induced oligodendrocyte apoptosis.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- SARS-CoV-2 mitochondriopathy in COVID-19 pneumonia exacerbates hypoxemia.Redox biology · 2022Article
- Molecular Mechanisms of SARS-CoV-2/COVID-19 Pathogenicity on the Central Nervous System: Bridging Experimental Probes to Clinical Evidence and Therapeutic Interventions.Advances in experimental medicine and biology · 2022Review
- Neuropathies and neurological dysfunction induced by coronaviruses.Journal of neurovirology · 2021Review
- Coronaviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines.Trends in immunology · 2020Review
- Neurobiology of coronaviruses: Potential relevance for COVID-19.Neurobiology of disease · 2020Review
- Article
- Pivotal Role of Receptor-Interacting Protein Kinase 1 and Mixed Lineage Kinase Domain-Like in Neuronal Cell Death Induced by the Human Neuroinvasive Coronavirus OC43.Journal of virology · 2017Article
- Gliopathy of Demyelinating and Non-Demyelinating Strains of Mouse Hepatitis Virus.Frontiers in cellular neuroscience · 2015Article
- Docetaxel induces moderate ovarian toxicity in mice, primarily affecting granulosa cells of early growing follicles.Molecular human reproduction · 2014Article
- ELR(+) chemokine signaling in host defense and disease in a viral model of central nervous system disease.Frontiers in cellular neuroscience · 2014Review
- Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways.Virus research · 2013Article
- Article
- Review
- Bax and calpain mediate excitotoxic oligodendrocyte death induced by activation of both AMPA and kainate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Human herpesvirus 6A induces apoptosis of HSB-2 cells via a mitochondrion-related caspase pathway.Journal of biomedical research · 2010Article
- Bid regulates the pathogenesis of neurotropic reovirus.PLoS pathogens · 2010Article
- CXCR2 signaling protects oligodendrocytes and restricts demyelination in a mouse model of viral-induced demyelination.PloS one · 2010Article
- Bid cleavage, cytochrome c release and caspase activation in canine coronavirus-induced apoptosis.Veterinary microbiology · 2010Article
- The pathogenesis of murine coronavirus infection of the central nervous system.Critical reviews in immunology · 2010Review
- The Biology of Persistent Infection: Inflammation and Demyelination following Murine Coronavirus Infection of the Central Nervous System.Current immunology reviews · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A previous study demonstrated that infection of rat oligodendrocytes by mouse hepatitis virus (MHV) resulted in apoptosis, which is caspase dependent (Y. Liu, Y. Cai, and X. Zhang, J. Virol. 77:11952-11963, 2003). Here we determined the involvement of the mitochondrial pathway in MHV-induced oligodendrocyte apoptosis. We found that caspase-9 activity was 12-fold higher in virus-infected cells than in mock-infected cells at 24 h postinfection (p.i.). Pretreatment of cells with a caspase-9 inhibitor completely blocked caspase-9 activation and partially inhibited the apoptosis mediated by MHV infection. Analyses of cytochrome c release further revealed an activation of the mitochondrial apoptotic pathway. Stable overexpression of the two antiapoptotic proteins Bcl-2 and Bcl-xL significantly, though only partially, blocked apoptosis, suggesting that activation of the mitochondrial pathway is partially responsible for the apoptosis. To identify upstream signals, we determined caspase-8 activity, cleavage of Bid, and expression of Bax and Bad by Western blotting. We found a drastic increase in caspase-8 activity and cleavage of Bid at 24 h p.i. in virus-infected cells, suggesting that Bid may serve as a messenger to relay the signals from caspase-8 to mitochondria. However, treatment with a caspase-8 inhibitor only slightly blocked cytochrome c release from the mitochondria. Furthermore, we found that Bax but not Bad was significantly increased at 12 h p.i. in cells infected with both live and UV-inactivated viruses and that Bax activation was partially blocked by treatment with the caspase-8 inhibitor. These results thus establish the involvement of the mitochondrial pathway in MHV-induced oligodendrocyte apoptosis.
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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.