ArticleMolecular medicine reports2019
Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- The aging mouse CNS is protected by an autophagy-dependent microglia population promoted by IL-34.Nature communications · 2024Article
- Molecular Mechanism of the Protective Effects of M2 Microglia on Neurons: A Review Focused on Exosomes and Secretory Proteins.Neurochemical research · 2022Review
- Platinum nanoparticles Protect Against Lipopolysaccharide-Induced Inflammation in Microglial BV-2 Cells via Decreased Oxidative Damage and Increased Phagocytosis.Neurochemical research · 2021Article
- Microglial Phenotypic Transition: Signaling Pathways and Influencing Modulators Involved in Regulation in Central Nervous System Diseases.Frontiers in cellular neuroscience · 2021Review
- Bruton's Tyrosine Kinase Inhibition Promotes Myelin Repair.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Rapamycin Alleviates the Symptoms of Multiple Sclerosis in Experimental Autoimmune Encephalomyelitis (EAE) Through Mediating the TAM-TLRs-SOCS Pathway.Frontiers in neurology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia were once thought to serve a pathogenic role in demyelinating diseases, particularly in multiple sclerosis (MS). However, it has recently been shown that in the experimental autoimmune encephalomyelitis (EAE) model of MS, microglia could serve a protective role by promoting remyelination via the efficient removal of apoptotic cells, the phagocytosis of debris and the support of myelinating oligodendrocytes. The aim of the present study was to determine if the effect of microglia could promote the recovery of EAE and attenuate symptoms in EAE. The severity of EAE was assessed by clinical scores, pathologic changes revealed by luxol fast blue staining and immunohistochemical techniques. The results suggested that microglia reduced clinical scores in mice, suppressed ongoing severe EAE and promoted remyelination and recovery in EAE mice. In addition, following induction with tuftsin, the M1/M2 cytokine balance was shifted, downregulating the proinflammatory M1 response and upregulating the anti‑inflammatory M2 response. Generally, microglia can stimulate remyelination, which serves a protective role in different phases of EAE and may represent a potential therapeutic strategy for the treatment of MS.
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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.