{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336612/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336612"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Effects of bile acid exposure on gene expression in oesophageal epithelial cells","description":"Gastro-oesophageal reflux disease is highly prevalent in systemic sclerosis (SSc) and may contribute to oesophageal tissue damage. To investigate the molecular effects of reflux-associated injury, human oesophageal epithelial cells (Het1A) were exposed to bile acids and analysed by RNA sequencing. Chronic bile acid exposure induced transcriptional changes associated with innate immune activation, type I interferon signalling, TGF-β responses, epithelial–mesenchymal transition (EMT), oxidative stress, and mitochondrial dysfunction. Differential gene expression profiles were compared with publicly available SSc oesophageal transcriptomic datasets to identify shared disease-associated pathways. These data provide insight into the molecular mechanisms by which bile acid-induced epithelial injury may contribute to oesophageal pathology in systemic sclerosis.","dates":{"publication":"2026/06/30"},"accession":"GSE336612","cross_references":{"GSM":["GSM9838820","GSM9838821","GSM9838816","GSM9838817","GSM9838818","GSM9838819"],"GPL":["9052"],"GSE":["336612"],"taxon":["Homo sapiens"]}}