CX3CR1-deficient microglia shows impaired signalling of the transcription factor NRF2: Implications in tauopathies
Open accessAbstract
TAU protein aggregation is the main characteristic of neurodegenerative diseases known as tauopathies. Low-grade chronic inflammation is also another hallmark that indicates crosstalk between damaged neurons and glial cells. Previously, we have demonstrated that neurons overexpressing TAUP301L release CX3CL1, which activates the transcription factor NRF2 signalling to limit over-activation in microglial cells in vitro and in vivo. However, the connection between CX3CL1/CX3CR1 and NRF2 system and its functional implications in microglia are poorly described. We evaluated CX3CR1/NRF2 axis in the context of tauopathies and its implication in neuroinflammation. Regarding the molecular mechanisms that connect CX3CL1/CX3CR1 and NRF2 systems, we observed that in primary microglia from Cx3cr1-/- mice the mRNA levels of Nrf2 and its related genes were significantly decreased, establishing a direct linking between both systems. To determine functional relevance of CX3CR1, migration and phagocytosis assays were evaluated. CX3CR1-deficient microglia showed impaired cell migration and deficiency of phagocytosis, as previously described for NRF2-deficient microglia, reinforcing the idea of the relevance of the CX3CL1/CX3CR1 axis in these events. The importance of these findings was evident in a tauopathy mouse model where the effects of sulforaphane (SFN), an NRF2 inducer, were examined on neuroinflammation in Cx3cr1+/+ and Cx3cr1-/- mice. Interestingly, the treatment with SFN was able to modulate astrogliosis but failed to reduce microgliosis in Cx3cr1-/- mice. These findings suggest an essential role of the CX3CR1/NRF2 axis in microglial function and in tauopathies. Therefore, polymorphisms with loss of function in CX3CR1 or NRF2 have to be taken into account for the development of therapeutic strategies.
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Tau can bind to microglial CX3CR1 and initiate the internalization and degradation of tau.
“Tau can bind to microglial CX3CR1 and initiate the internalization and degradation of tau [191].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [191]
CX3CL1 competes with tau for binding to CX3CR1, leading to a decrease in the internalization of tau.
“CX3CL1 competes with tau for binding to CX3CR1, leading to a decrease in the internalization of tau.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [191]
Phosphorylated tau at Ser396 exhibits reduced binding affinity to CX3CR1.
“In addition, phosphorylated tau at Ser396 exhibits reduced binding affinity to CX3CR1 [191].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [191]
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Simpson, D. S. A., & Oliver, P. L. (2020) · Antioxidants · doi:10.3390/antiox9080743 · Cited by 1,044 · see citing works
Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation
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- Authors
- Castro-Sánchez, S., García-Yagüe, Á. J., Kügler, S., & Lastres-Becker, I.
- Affiliations
- Universitätsmedizin Göttingen (DE)
- ORCID
- Kügler, Sebastian
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 22
- Pages
- 101118
- ISSN
- 2213-2317 (ISSN-L)
- PMC
- PMC6375000
- OpenAlex
- W2913929619
- Cited by
- 76
- References
- 73
- Citations by year
- 2026: 9 · 2025: 18 · 2024: 12 · 2023: 5 · 2022: 9 · 2021: 10 · 2020: 10 · 2019: 3
- FWCI
- 3.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Redox Biology (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Biblos-e Archivo (Universidad Autónoma de Madrid) (submittedVersion, cc-by-nc-nd)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Hispana (submittedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
- Funders
- Spanish Ministry of Economy and Competitiveness (SAF2016-76520-R)
- 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
- CX3CR1, Nrf2, fractalkine, tauopathy, microglia, neuroinflammation, sulforaphane, microglial migration, phagocytosis, astrocyte activation, microglial activation, tau aggregation, neurodegenerative diseases, loss-of-function polymorphism
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Cell Line, Cell Movement, Disease Models, Animal, Disease Susceptibility, Gene Expression Regulation, Humans, Phagocytosis, RNA, Messenger, Signal Transduction, Gene Expression, tau Proteins, Microglia, Pyramidal Cells, Mice, Knockout, Tauopathies, NF-E2-Related Factor 2, Mice
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Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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