{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE322nnn/GSE322756/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE322756"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Effects of nickel ion treatment on gene expression during osteogenic differentiation of mouse bone marrow mesenchymal stem cells","description":"Nickel (Ni) is a ubiquitous environmental trace metal, yet its physiological roles and dose-dependent effects in skeletal biology remain poorly understood. Through comprehensive in vivo and in vitro experiments, we demonstrated that low-dose Ni (0.1 μM) significantly enhances matrix mineralization during osteogenic differentiation, whereas this pro-mineralization effect is markedly attenuated at higher concentrations. Although the inhibitory mechanism of high-dose nickel on osteogenesis has been largely attributed to oxidative stress, the molecular basis underlying the promotional effect of low-dose nickel remains unclear. To address this, we performed RNA-seq analysis on primary mouse bone marrow mesenchymal stem cells (mBMSCs) treated with 0.1 μM nickel following 7 days of osteogenic induction, aiming to elucidate the downstream signaling pathways responsible for its beneficial effects on bone mineralization.","dates":{"publication":"2026/06/03"},"accession":"GSE322756","cross_references":{"GSM":["GSM9557808","GSM9557807","GSM9557809","GSM9557804","GSM9557806","GSM9557805"],"GPL":["24247"],"GSE":["322756"],"taxon":["Mus musculus"],"PMID":["[42196516]"]}}