{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335283/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE335283"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Hemin Impairs Interferon Signaling in Periodontal Cells","description":"Hemin has been shown to exert potent immunomodulatory effects in the oral microenvironment, yet its global transcriptional targets remain elusive. In this study, we performed high-throughput Bulk RNA-sequencing to investigate the transcriptomic reprogramming induced by Hemin in human oral epithelial cells (HSC-2) under inflammatory conditions. Our transcriptomic analysis revealed that Hemin effectively reversed the inflammatory signature induced by IL-1β and TNF-α. Specifically, Hemin treatment profoundly and selectively paralyzed the interferon (IFN)-stimulated gene axis (e.g., CXCL10, CXCL11), alongside triggering compensatory NRF2-driven redox stress defenses (e.g., HMOX1). These RNA-seq data provide a comprehensive landscape demonstrating Hemin's role as a targeted repressor that fundamentally uncouples JAK-STAT interferon responses.","dates":{"publication":"2026/06/17"},"accession":"GSE335283","cross_references":{"GSM":["GSM9809388","GSM9809389","GSM9809386","GSM9809387","GSM9809391","GSM9809380","GSM9809381","GSM9809390","GSM9809384","GSM9809385","GSM9809382","GSM9809383"],"GPL":["11154"],"GSE":["335283"],"taxon":["Homo sapiens"]}}