ArticleJournal of molecular neuroscience : MN2013
Abnormal activation of microglia accompanied with disrupted CX3CR1/CX3CL1 pathway in the brains of the hamsters infected with scrapie agent 263K.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- A critical appraisal on the involvement of plant-based extracts as neuroprotective agents (2012-2022): an effort to ease out decision-making process for researchers.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Molecular signatures in prion disease: altered death receptor pathways in a mouse model.Journal of translational medicine · 2024Article
- Effects of Antiretroviral Treatment on Central and Peripheral Immune Response in Mice with EcoHIV Infection.Cells · 2024Article
- Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPMolecular neurobiology · 2022Article
- Activation of Innate Immunity and Autophagy in Brain Tissues with Prion Disease and Degradation of Abnormal PrPs in Cells - China's Studies.China CDC weekly · 2022Review
- MiR-146b-5p/TRAF6 axis is essential forFrontiers in pharmacology · 2022Article
- The role of microglia in prion diseases and possible therapeutic targets: a literature review.Prion · 2021Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Review
- Impact of COVID-19 Pandemic on Patients With Neurodegenerative Diseases.Frontiers in aging neuroscience · 2021Review
- The Use of Ginkgo Biloba L. as a Neuroprotective Agent in the Alzheimer's Disease.Frontiers in pharmacology · 2021Review
- IP10, KC and M-CSF Are Remarkably Increased in the Brains from the Various Strains of Experimental Mice Infected with Different Scrapie Agents.Virologica Sinica · 2020Article
- Assessment of Glial Activation Response in the Progress of Natural Scrapie after Chronic Dexamethasone Treatment.International journal of molecular sciences · 2020Article
- Phagocytosis of full-length Tau oligomers by Actin-remodeling of activated microglia.Journal of neuroinflammation · 2020Article
- Combinatory FK506 and Minocycline Treatment Alleviates Prion-Induced Neurodegenerative Events via Caspase-Mediated MAPK-NRF2 Pathway.International journal of molecular sciences · 2019Article
- Microglia in neurodegeneration.Nature neuroscience · 2018Review
- Different Molecular Mechanisms Mediate Direct or Glia-Dependent Prion Protein Fragment 90-231 Neurotoxic Effects in Cerebellar Granule Neurons.Neurotoxicity research · 2017Article
- Remarkable increases of α1-antichymotrypsin in brain tissues of rodents during prion infection.Prion · 2017Article
- Microglia in prion diseases.The Journal of clinical investigation · 2017Review
- Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases.Molecular neurobiology · 2017Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglial cells are resident mononuclear phagocytes of the central nervous system (CNS). Active proliferation of microglia in the brain has been identified in neurodegenerative disorders, including some kinds of prion disease. However, the detailed regional distribution between microglia and PrP(Sc) deposition has not been presented, and investigation of fractalkine signaling which is involved in the regulation of activation of microglia in prion disease is not well documented. In this study, the disease phenomenon of microglial accumulation in the CNS was thoroughly analyzed using a scrapie-infected experimental model. Western blots of microglia-specific markers Iba1 and CD68, immunohistochemical and immunofluorescent assays demonstrated obviously activation of microglia in almost whole brain regions in the infected animals. Under the dynamic analysis on hallmarks of activation of microglia, a time-dependent increase of Iba1 and CD68 was detected, accompanied by accumulation of PrP(Sc) and progression of neurodegenerative symptoms. With serial brain sections and double staining of Iba1 and PrP(Sc), we observed that the microglia distributed around PrP(Sc) deposits in 263K-infected hamsters' brains, proposing PrP(Sc) phagocytosis. Flow cytometry assays with the single-cell suspensions prepared from the cortical region of the infected brains verified an activation of microglial population. ELISA assays of the cytokines in brain homogenates revealed significant upregulations of interleukin (IL)-1β, IL-6 and TNF-α when infected. Evaluation of fractalkine signaling in the infected hamsters' brains showed progressively downregulation of CX3CL1 during the incubation. Prion peptide PrP106-126 also disrupted fractalkine and evoked microglial activation in rat primary neuron-glia mixed cultures. Our data here demonstrate an activated status of microglia in CNS tissues of infectious prion disease, possibly through fractalkine signaling deficiency.
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