0000000001188873
AUTHOR
Francesc Ibáñez
TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles
Background Current evidence indicates that extracellular vesicles (EVs) participate in intercellular signaling, and in the regulation and amplification of neuroinflammation. We have previously shown that ethanol activates glial cells through Toll-like receptor 4 (TLR4) by triggering neuroinflammation. Here, we evaluate if ethanol and the TLR4 response change the release and inflammatory content of astrocyte-derived EVs, and whether these vesicles are capable of communicating with neurons by spreading neuroinflammation. Methods Cortical neurons and astrocytes in culture were used. EVs were isolated from the extracellular medium of the primary culture of the WT and TLR4-KO astrocytes treated …
Circulating MicroRNAs in Extracellular Vesicles as Potential Biomarkers of Alcohol-Induced Neuroinflammation in Adolescence: Gender Differences
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Exosomes as mediators of neuron-glia communication in neuroinflammation
In recent years, a type of extracellular vesicles named exosomes has emerged that play an important role in intercellular communication under physiological and pathological conditions. These nanovesicles (30–150 nm) contain proteins, RNAs and lipids, and their internalization by bystander cells could alter their normal functions. This review focuses on recent knowledge about exosomes as messengers of neuron-glia communication and their participation in the physiological and pathological functions in the central nervous system. Special emphasis is placed on the role of exosomes under toxic or pathological stimuli within the brain, in which the glial exosomes containing inflammatory molecules…
Additional file 4: of TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles
Table S1. Nucleotide sequences of the primers used for the TaqMan RT-qPCR of miRNAs. Table S2. Nucleotide sequences of the primers used for the RT-PCR of genes. Table S3. Targets for mmu-mir-146a, mmu-mir-182 and mmu-mir-200b obtained by the mirnet.es webserver. Table S4. The KEGG pathways obtained by the DIANA tool webserver. Table S5. The KEGG pathways that derived from the String protein-protrin interaction analysis between the target genes modulated by mmu-miR-146a and mmu-mir-182. (DOCX 57 kb)
Additional file 3: of TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles
Figure S3. Analysis of the RNA population isolated from the WT and TLR4-KO, ethanol-treated or not astrocyte-derived EVs by a 2100 Agilent Bioanalyzer. X axis shows the nucleotide length of the RNA population and the Y axis its fluorescence intensity. (TIF 366 kb)
Additional file 2: of TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles
Figure S2. A) Flow cytometry graph of a mixture of FITC fluorescent beads with different diameters of 100 nm, 300 nm, 500 nm and 900 nm (Megamix-Plus FSC beads), which was used to detect the EVs obtained from the WT and TLR4-KO astrocytes. B) Example of the graph obtained in the nanoparticles tracking analysis using size distribution and the concentration of microvesicles. (TIF 924 kb)
Additional file 1: of TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles
Figure S1. Immunoblot analysis of the calnexin levels present in the EVs from the untreated and ethanol-treated WT and TLR4-KO astrocytes. The absence of the calnexin expression in the exosome samples confirmed the absence of cytosolic protein contamination. A sample of astrocyte lysate was used as positive control of the calnexin expression. (TIF 489 kb)