<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/GSE303nnn/GSE303528/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></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=GSE303528</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA Sequencing Reveals Differential Gene Expression in Human Brain Microvascular Endothelial Cells (HBMECs) Subjected to Oxygen-Glucose Deprivation/Reperfusion (OGD/R)</name><description>Human brain microvascular endothelial cells (HBMECs) are a critical component of the blood-brain barrier (BBB), and their stability is paramount for BBB integrity, particularly under pathological stress such as ischemic stroke. This study employed an *in vitro* model of ischemia-reperfusion injury using oxygen-glucose deprivation followed by reperfusion (OGD/R) on cultured HBMECs. To comprehensively characterize the transcriptional response, we performed high-throughput RNA sequencing (RNA-seq) on both OGD/R-treated and control (normoxic) HBMEC samples. Our analysis identified a significant number of differentially expressed genes (DEGs) associated with the OGD/R challenge. These DEGs encompass genes involved in key biological processes pertinent to endothelial cell dysfunction, BBB disruption, inflammatory responses, oxidative stress, apoptosis, and potential protective/repair mechanisms. This dataset provides a detailed transcriptional profile of HBMECs undergoing simulated ischemia-reperfusion injury. It serves as a valuable resource for elucidating the molecular mechanisms underlying BBB compromise in ischemic stroke and for identifying novel potential therapeutic targets aimed at preserving BBB function and mitigating neuronal damage.</description><dates><publication>2026/06/30</publication></dates><accession>GSE303528</accession><cross_references><GSM>GSM9128531</GSM><GSM>GSM9128532</GSM><GSM>GSM9128533</GSM><GSM>GSM9128534</GSM><GSM>GSM9128535</GSM><GSM>GSM9128536</GSM><GPL>24676</GPL><GSE>303528</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>