{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339142/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339142"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Fibronectin inhibition restores myelination in endothelial TNFR2-depedent non-remitting Experimental Autoimmune Encephalomyelitis [snRNA-Seq]","description":"Multiple Sclerosis (MS) is characterized by impaired remyelination and progressive neurodegeneration. We investigated the mechanisms underlying remyelination failure in Experimental Autoimmune Encephalomyelitis (EAE), a murine model of MS. TNFR2 deletion induces a severe non-remitting disease course and the main aim was to identify the cell population that drives this phenomenon. Through the analysis of single-nucleus RNA sequencing datasets, we identified endothelial cell-specific TNFR2 ablation as a driver of impaired remyelination. This effect was associated with fibronectin overexpression and accumulation in demyelinating lesions, highlighting the critical role of endothelial-specific TNFR2 signaling in central nervous system repair.","dates":{"publication":"2026/09/07"},"accession":"GSE339142","cross_references":{"GSM":["GSM9889062","GSM9889061","GSM9889060","GSM9889063","GSM9889059","GSM9889058"],"GPL":["28457"],"GSE":["339142"],"taxon":["Mus musculus"]}}