<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/GSE339nnn/GSE339100/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</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=GSE339100</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>sc-RNAseq of glomerular cells in a mouse model of malignant hypertension</name><description>Hypertensive emergency (HTEM) is defined by abrupt blood pressure elevation with acute multi‑organ damage, yet the mechanisms predisposing only a subset of hypertensive individuals to HTEM remain unclear. Progress has been limited by the lack of a mouse model that faithfully replicates human disease. We aimed to identify determinants of susceptibility to hypertensive microvascular injury and characterize a murine model of HTEM. Males 129S2/SvPasCrl (129Sv) mice were exposed to severe hypertension via angiotensin II infusion combined with a high‑salt diet wth or withour supplementation with rhPlGF2. We assessed glomerular transcriptional profiles using single‑cell RNA sequencing. Single‑cell transcriptomics revealed profound repression of angiogenic, metabolic, and stress-response pathways in glomerular endothelial cells, a repression partially restored by rhPlGF-2.</description><dates><publication>2026/09/01</publication></dates><accession>GSE339100</accession><cross_references><GSM>GSM9888482</GSM><GSM>GSM9888483</GSM><GSM>GSM9888480</GSM><GSM>GSM9888481</GSM><GSM>GSM9888479</GSM><GSM>GSM9888477</GSM><GSM>GSM9888478</GSM><GPL>30172</GPL><GSE>339100</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>