{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee HG"],"funding":["NIAID NIH HHS","NIEHS NIH HHS","NIMH NIH HHS","NINDS NIH HHS","NIGMS NIH HHS"],"pagination":["865-872"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11016191"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["627(8005)"],"pubmed_abstract":["Disease-associated astrocyte subsets contribute to the pathology of neurologic diseases, including multiple sclerosis and experimental autoimmune encephalomyelitis<sup>1-8</sup> (EAE), an experimental model for multiple sclerosis. However, little is known about the stability of these astrocyte subsets and their ability to integrate past stimulation events. Here we report the identification of an epigenetically controlled memory astrocyte subset that exhibits exacerbated pro-inflammatory responses upon rechallenge. Specifically, using a combination of single-cell RNA sequencing, assay for transposase-accessible chromatin with sequencing, chromatin immunoprecipitation with sequencing, focused interrogation of cells by nucleic acid detection and sequencing, and cell-specific in vivo CRISPR-Ca"],"journal":["Nature"],"pubmed_title":["Disease-associated astrocyte epigenetic memory promotes CNS pathology."],"pmcid":["PMC11016191"],"funding_grant_id":["R01 NS102807","R01 MH130458","R00 NS114111","R01 ES029136","T32 GM007356","DP2 AI154435","K22 AI152644","R01 MH132632","R01 AI126880"],"pubmed_authors":["Akl CF","Giovannoni F","Kenison JE","Prat A","Piester G","Clark IC","Charabati M","Rothhammer V","Pernin F","Quintana FJ","Rone JM","Illouz T","Kleemann KL","Chao CC","Wheeler MA","Li Z","Antel JP","Srun L","Sanmarco LM","Shin SW","Zandee SEJ","Lee HG","Flausino LE","Lee JH"],"additional_accession":[]},"is_claimable":false,"name":"Disease-associated astrocyte epigenetic memory promotes CNS pathology.","description":"Disease-associated astrocyte subsets contribute to the pathology of neurologic diseases, including multiple sclerosis and experimental autoimmune encephalomyelitis<sup>1-8</sup> (EAE), an experimental model for multiple sclerosis. However, little is known about the stability of these astrocyte subsets and their ability to integrate past stimulation events. Here we report the identification of an epigenetically controlled memory astrocyte subset that exhibits exacerbated pro-inflammatory responses upon rechallenge. Specifically, using a combination of single-cell RNA sequencing, assay for transposase-accessible chromatin with sequencing, chromatin immunoprecipitation with sequencing, focused interrogation of cells by nucleic acid detection and sequencing, and cell-specific in vivo CRISPR-Ca","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-08-14T03:05:39.822Z","creation":"2025-04-20T00:11:20.996Z"},"accession":"S-EPMC11016191","cross_references":{"pubmed":["38509377"],"doi":["10.1038/s41586-024-07187-5"]}}