ArticleJournal of neuroinflammation2015
Role of glial 14-3-3 gamma protein in autoimmune demyelination.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Astrocyte-related proteins mediate the association of YWHAG with Alzheimer's pathology and enhance its diagnostic value.Translational psychiatry · 2026Article
- Systematic Analysis of Alternative Splicing in Transcriptomes of Multiple Sclerosis Patient Brain Samples.International journal of molecular sciences · 2025Article
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- Article
- Pathways to Parkinson's disease: a spotlight on 14-3-3 proteins.NPJ Parkinson's disease · 2021Review
- Emerging roles of 14-3-3γ in the brain disorder.BMB reports · 2020Review
- Dysregulation of peripheral expression of the YWHA genes during conversion to psychosis.Scientific reports · 2020Article
- 14-3-3γ Haploinsufficient Mice Display Hyperactive and Stress-sensitive Behaviors.Experimental neurobiology · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe family of 14-3-3 proteins plays an important role in the regulation of cell survival and death. Here, we investigate the role of the 14-3-3 gamma (14-3-3 γ) subunit for glial responses in autoimmune demyelination.
methodsExpression of 14-3-3 γ in glial cell culture was investigated by reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemistry. 14-3-3 γ knockout mice were subjected to murine myelin oligodendrocyte-induced experimental autoimmune encephalomyelitis (MOG-EAE), an animal model mimicking inflammatory features and neurodegenerative aspects of multiple sclerosis (MS).
resultsExpression studies in cell culture confined expression of 14-3-3 γ to both, oligodendrocytes (OL) and astrocytes. RT-PCR analysis revealed an increased expression of 14-3-3 γ mRNA in the spinal cord during the late chronic phase of MOG-EAE. At that stage, EAE was more severe in 14-3-3 γ knockout mice as compared to age- and gender-matched controls. Histopathological analyses on day 56 post immunization (p.i.) revealed significantly enhanced myelin damage as well as OL injury and secondary, an increase in axonal injury and gliosis in 14-3-3 γ -/- mice. At the same time, deficiency in 14-3-3 γ protein did not influence the immune response. Further histological studies revealed an increased susceptibility towards apoptosis in 14-3-3 γ-deficient OL in the inflamed spinal cord.
conclusionThese data argue for a pivotal role of 14-3-3 γ-mediated signalling pathways for OL protection in neuroinflammation.
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