Expression of Tau40 Induces Activation of Cultured Rat Microglial Cells
Open accessAbstract
Accumulation of microtubule-associated protein tau has been observed in the brain of aging and tauopathies. Tau was observed in microglia, but its role is not illustrated. By immunofluorescence staining and the fractal dimension value assay in the present study, we observed that microglia were activated in the brains of rats and mice during aging, simultaneously, the immunoreactivities of total tau and the phosphorylated tau were significantly enhanced in the activated microglia. Furtherly by transient transfection of tau40 (human 2N/4R tau) into the cultured rat microglia, we demonstrated that expression of tau40 increased the level of Iba1, indicating activation of microglia. Moreover, expression of tau40 significantly enhanced the membranous localization of the phosphorylated tau at Ser396 in microglia possibly by a mechanism involving protein phosphatase 2A, extracellular signal-regulated kinase and glycogen synthase kinase-3β. It was also found that expression of tau40 promoted microglial migration and phagocytosis, but not proliferation. And we observed increased secretion of several cytokines, including interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor-α and nitric oxide after the expression of tau40. These data suggest a novel role of human 2N/4R tau in microglial activation.
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Tau-dependent microglial activation enhances secretion of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α.
“Tau-dependent microglial activation can enhance secretion of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α [421–423].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [421]
Overexpression of full-length tau in cultured rat microglia caused their activation.
“Thirdly, when applied in vitro, overexpression of full-length tau in cultured rat microglia caused their activation.382”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [382]
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References 92 · Cited by 47
- Authors
- Wang, L., Jiang, Q., Chu, J., Lin, L., Li, X.-G., Chai, G.-S., Wang, Q., Wang, J.-Z., & Tian, Q.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Corresponding author
- Wang, Jian-Zhi
- Tian, Qing
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-10-11
- Volume
- 8
- Issue
- 10
- Pages
- e76057
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3795725
- OpenAlex
- W2090858540
- Cited by
- 47
- References
- 92
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 4 · 2021: 5 · 2020: 8 · 2019: 7 · 2018: 3 · 2017: 2 · 2016: 4 · 2015: 6 · 2014: 2
- FWCI
- 2.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (30971204, 81271404)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- tau protein, microglial activation, microglia, tau phosphorylation, protein phosphatase 2A, ERK, glycogen synthase kinase-3β, microglial migration, phagocytosis, cytokine production, aging, tauopathy, Iba1
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Animals, Calcium-Binding Proteins, Cell Movement, Cells, Cultured, Gene Expression Regulation, Humans, Male, Membrane Proteins, Microfilament Proteins, Nitric Oxide, Phagocytosis, Tumor Necrosis Factor-alpha, Signal Transduction, Interleukin-6, Interleukin-10, tau Proteins, Rats, Sprague-Dawley, Microglia, Glycogen Synthase Kinase 3, Extracellular Signal-Regulated MAP Kinases, p38 Mitogen-Activated Protein Kinases, Rats, Interleukin-1beta, Protein Phosphatase 2
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