{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Xlsx":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE298nnn/GSE298536/suppl/GSE298536_normalized_counts.xlsx"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE298nnn/GSE298536/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Rattus norvegicus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE298536"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Preservation of Myogenic Tone in Kidney Microvasculature of Dahl Salt-Sensitive Rats. Role of C-C motif chemokine ligand 2","description":"Kidney injury mechanisms that develop in salt-sensitive (SS) hypertension are incompletely understood. Using the Dahl SS rat, which is a prominent model of salt-sensitive hypertension and associated kidney injury, loss of function of the pro-inflammatory transcription factor, ETS-1, corrects kidney microvascular autoregulatory dysfunction and injury. C-C motif chemokine ligand 2 (CCL2) is a direct target of ETS-1, so SS rats lacking Ccl2 (termed (SSCcl2 -/-) were therefore examined. Unlike SS rats, SSCcl2 -/- rats did not develop salt-sensitive hypertension, loss of autoregulation of afferent arterioles, or kidney injury. cDNA libraries from renal microvasculature of these rats was sequenced.","dates":{"publication":"2026/04/02"},"accession":"GSE298536","cross_references":{"GSM":["GSM9016430","GSM9016431","GSM9016420","GSM9016421","GSM9016432","GSM9016433","GSM9016422","GSM9016423","GSM9016424","GSM9016425","GSM9016414","GSM9016426","GSM9016415","GSM9016427","GSM9016416","GSM9016428","GSM9016417","GSM9016429","GSM9016418","GSM9016419"],"GPL":["20084"],"GSE":["298536"],"taxon":["Rattus norvegicus"],"PMID":["[41833640]"]}}