{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330702/"]},"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=GSE330702"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"RNA-seq analysis of Nogo-B knockdown in human dermal lymphatic endothelial cells under TGF-β2 stimulation","description":"Nogo-B (RTN4B), an endoplasmic reticulum-associated protein, plays a critical role in regulating endothelial cell function and vascular remodeling. However, its role in lymphatic endothelial cells (LECs) and in response to profibrotic signaling remains poorly understood. Transforming growth factor-β2 (TGF-β2) is a key regulator of endothelial phenotypes and has been implicated in lymphatic dysfunction under pathological conditions. In this study, we performed RNA sequencing (RNA-seq) to investigate the transcriptional changes associated with Nogo-B knockdown in human dermal lymphatic endothelial cells (HDLECs) under TGF-β2 stimulation. HDLECs were transduced with shRNA targeting Nogo-B (shNogo-B) or control shRNA (shGFP), followed by treatment with TGF-β2 for 72 hours. Total RNA was extracted and subjected to high-throughput sequencing. Comparative transcriptomic analysis was conducted to identify differentially expressed genes and pathways regulated by Nogo-B under TGF-β2-stimulated conditions. This dataset provides insights into the molecular mechanisms by which Nogo-B modulates lymphatic endothelial cell responses to TGF-β signaling, including pathways related to extracellular matrix organization, cell migration, proliferation, and cytoskeletal remodeling. These data serve as a resource for understanding the role of Nogo-B in lymphatic endothelial biology and its contribution to TGF-β-mediated signaling and dysfunction.","dates":{"publication":"2026/05/13"},"accession":"GSE330702","cross_references":{"GSM":["GSM9730777","GSM9730776","GSM9730775","GSM9730774","GSM9730779","GSM9730778","GSM9730780","GSM9730773","GSM9730772","GSM9730782","GSM9730771","GSM9730781"],"GPL":["24676"],"GSE":["330702"],"taxon":["Homo sapiens"]}}