<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330702/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE330702</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA-seq analysis of Nogo-B knockdown in human dermal lymphatic endothelial cells under TGF-β2 stimulation</name><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.</description><dates><publication>2026/05/13</publication></dates><accession>GSE330702</accession><cross_references><GSM>GSM9730777</GSM><GSM>GSM9730776</GSM><GSM>GSM9730775</GSM><GSM>GSM9730774</GSM><GSM>GSM9730779</GSM><GSM>GSM9730778</GSM><GSM>GSM9730780</GSM><GSM>GSM9730773</GSM><GSM>GSM9730772</GSM><GSM>GSM9730782</GSM><GSM>GSM9730771</GSM><GSM>GSM9730781</GSM><GPL>24676</GPL><GSE>330702</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>