Regulation of IL-6 secretion by astrocytes via TLR4 in the fragile X mouse model.
Open accessAbstract
Fragile X syndrome (FXS) is identified by abnormal dendrite morphology and altered synaptic protein expression. Astrocyte secreted factors such as Tenascin C (TNC), may contribute to the synaptic changes, including maturation of the synapse. TNC is a known endogenous ligand of toll-like receptor 4 (TLR4) that has been shown to induce the expression of pro-inflammatory cytokines such as interleukin-6 (IL-6). At the molecular level, elevated IL-6 promotes excitatory synapse formation and increases dendrite spine length. With these molecular changes linked to the phenotype of FXS, we examined the expression and the mechanism of the endogenous TLR4 activator TNC, and its downstream target IL-6 in astrocytes from the FMR1 KO mouse model. Secreted TNC and IL-6 were significantly increased in FMR1 KO astrocytes. Addition of TNC and lipopolysaccharide (LPS) induced IL-6 secretion, whereas the antagonist of TLR4 (LPS-RS) had an opposing effect. Cortical protein expression of TNC and IL-6 were also significantly elevated in the postnatal FMR1 KO mouse. In addition, there was an increase in the number of VGLUT1/PSD95 positive synaptic puncta of both WT and FMR1 KO neurons when plated with astrocyte conditioned media from FMR1 KO astrocytes, compared to those plated with media from wild type astrocytes. By assessing the cellular mechanisms involved, a novel therapeutic option could be made available to target abnormalities of synaptic function seen in FXS.
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Tenascin C (TNC), an activator of TLR4 that can promote excitatory synapse formation and immature spine morphology, is overexpressed in Fmr1 KO astrocytes.
“Tenascin C (TNC), an activator of TLR4 that can promote excitatory synapse formation and immature spine morphology, is overexpressed in Fmr1 KO astrocytes (Krasovska and Doering, 2018).”
From Astrocytes in fragile X syndrome (2024) · cites this paper as Krasovska and Doering, 2018
The Results section (page not available) reports increased cell-associated and secreted TNC in FMR1 KO astrocytes. The Introduction and Discussion describe TNC as a TLR4 activator and a possible contributor to excitatory synapse development, but they do not establish that TNC promotes immature spine morphology. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTLR4/MyD88-mediated induction of IL-6 is overactive in Fmr1 KO astrocytes, implicating involvement of inflammatory factors and suggesting alteration in TLR4/MyD88/PI3K interactions in FXS astrocytes.
“TLR4/MyD88-mediated induction of IL-6 is overactive in Fmr1 KO astrocytes (Krasovska and Doering, 2018), implicating involvement of inflammatory factors and suggesting alteration in TLR4/MyD88/PI3K interactions (Laird et al., 2009) in FXS astrocytes.”
From Astrocytes in fragile X syndrome (2024) · cites this paper as Krasovska and Doering, 2018
The Abstract reports elevated secreted IL-6 in FMR1 KO astrocytes, and the Discussion (WT and FMR1 KO Astrocyte Response to Immunological Challenges; page unavailable) reports that TLR4 antagonism reduced their IL-6 secretion. But the paper does not establish overactive MyD88-mediated induction in KO astrocytes: it cites another study for MyD88 dependence and reports that KO cells responded less than WT cells to some TLR4 stimuli. The later suggestion about PI3K interactions is attached to a different citation in the citing sentence. (LLM, conf=0.86)
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Astrocytic contribution to auditory hypersensitivity in a mouse model of fragile X syndromePreprint
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Local Translation in Glial Cells of the Brain
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- Authors
- Krasovska, V., & Doering, L. C.
- Affiliations
- McMaster University (CA)
- Corresponding author
- Doering, Laurie C.
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-08-03
- Volume
- 11
- Pages
- 272-272
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC6085486
- OpenAlex
- W2886733693
- Cited by
- 47
- References
- 48
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 6 · 2023: 5 · 2022: 7 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 1
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Molecular Neuroscience (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)
- Funders
- Fondation Brain Canada
- Azrieli Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- fragile X syndrome, astrocytes, interleukin-6, tenascin-C, TLR4, Fmr1 knockout mice, dendritic spine morphology, excitatory synapse formation, astrocyte-neuron interaction, lipopolysaccharide, VGLUT1, PSD-95, inflammatory cytokines
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