GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301517/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301517GEOGSEfalseChromatin topology dynamics of dexamethasone-treated trabecular meshwork identifies 78 causal genes for intraocular pressure and primary open angle glaucoma [RNA-seq]The physiology of trabecular meshwork (TM) controls aqueous humor outflow resistance and thereby intraocular pressure (IOP), a major risk factor for primary open-angle glaucoma (POAG). To decipher how GWAS-identified non-coding variants contribute to IOP and POAG, we generated a high-resolution map of genome topology and regulatory modules from primary human TM cell lines. Integrated analyses with dexamethasone-treated TM cells, a model of augmented IOP, demonstrate extensive changes in chromatin compartments, accessibility, looping, and histone marks that are highly concordant with transcriptional changes. By combining GWAS-associated variants with dexamethasone-induced chromatin looping, we discovered 26 IOP- and 52 POAG- candidate causal genes, belonging to key TM pathways, including integrin, transcriptional regulation of VENTX, and TNF signaling. Our studies provide a mechanistic framework for elucidating genetic complexity of IOP and pathogenesis of POAG and suggest new targets for therapies.2026/04/10GSE301517GSM9084589GSM9084578GSM9084579GSM9084598GSM9084587GSM9084588GSM9084592GSM9084581GSM9084582GSM9084593GSM9084590GSM9084591GSM9084580GSM9084596GSM9084585GSM9084597GSM9084586GSM9084594GSM9084583GSM9084595GSM908458430173301517Homo sapiens[41890121]