ArticleThe EMBO journal2000
Targeted expression of baculovirus p35 caspase inhibitor in oligodendrocytes protects mice against autoimmune-mediated demyelination.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 101 citations in OpenAlex.
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells · 2024Review
- Protective Effects of a Nano-Formulation of Curcumin against Cuprizone-Induced Demyelination in the Mouse Corpus Callosum.Iranian journal of pharmaceutical research : IJPR · 2020Article
- Sephin1, which prolongs the integrated stress response, is a promising therapeutic for multiple sclerosis.Brain : a journal of neurology · 2019Article
- Article
- NF-κB Activation Protects Oligodendrocytes against Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Creatine Enhances Mitochondrial-Mediated Oligodendrocyte Survival After Demyelinating Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model.Nature communications · 2016Article
- Harnessing the integrated stress response for the treatment of multiple sclerosis.The Lancet. Neurology · 2016Review
- Pharmaceutical integrated stress response enhancement protects oligodendrocytes and provides a potential multiple sclerosis therapeutic.Nature communications · 2015Article
- The unfolded protein response in multiple sclerosis.Frontiers in neuroscience · 2015Review
- Finding degrees of separation: experimental approaches for astroglial and oligodendroglial cell isolation and genetic targeting.Journal of neuroscience methods · 2014Review
- Article
- Oligodendrocyte-specific activation of PERK signaling protects mice against experimental autoimmune encephalomyelitis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Baculovirus infection triggers a shift from amino acid starvation-induced autophagy to apoptosis.PloS one · 2012Article
- Molecular mechanisms of oligodendrocyte injury in multiple sclerosis and experimental autoimmune encephalomyelitis.International journal of molecular sciences · 2012Review
- Neuroprotection by ulinastatin in experimental autoimmune encephalomyelitis.Neurochemical research · 2011Article
- Overexpression of the dominant-negative form of interferon regulatory factor 1 in oligodendrocytes protects against experimental autoimmune encephalomyelitis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Schwann-spheres derived from injured peripheral nerves in adult mice--their in vitro characterization and therapeutic potential.PloS one · 2011Article
- Article
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13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms underlying oligodendrocyte (OLG) loss and the precise roles played by OLG death in human demyelinating diseases such as multiple sclerosis (MS), and in the rodent model of MS, experimental autoimmune encephalomyelitis (EAE), remain to be elucidated. To clarify the involvement of OLG death in EAE, we have generated transgenic mice that express the baculovirus anti-apoptotic protein p35 in OLGs through the Cre-loxP system. OLGs from cre/p35 transgenic mice were resistant to tumor necrosis factor-alpha-, anti-Fas antibody- and interferon-gamma-induced cell death. cre/p35 transgenic mice were resistant to EAE induction by immunization with the myelin oligodendrocyte glycoprotein. The numbers of infiltrating T cells and macrophages/microglia in the EAE lesions were significantly reduced, as were the numbers of apoptotic OLGs expressing the activated form of caspase-3. Thus, inhibition of apoptosis in OLGs by p35 expression alleviated the severity of the neurological manifestations observed in autoimmune demyelinating diseases.
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