<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/GSE275nnn/GSE275703/</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=GSE275703</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Silicon Nitride Induces Osteoconduction Via Activated Mitochondrial Oxidative Phosphorylation and Neovascularization</name><description>Silicon Nitride (Si3N4: SiN) is a thermodynamically stable ceramic material with excellent mechanical properties and wear/corrosion resistance for industrial applications. SiN is also proposed for orthopedic and dental implant applications because of its enhanced osteoconduction. However, the biological mechanism of SiN-induced bone formation has not been fully elucidated. In this study, SiN significantly increased in vitro mineralization of human bone marrow mesenchymal stromal cells (BM-MSC) and in vivo peri-implant bone volume in mouse femurs over conventionally used titanium (Ti) implants. RNA sequencing of BM-MSC cultured on SiN disc revealed that the functional gene clusters associated with mitochondrial oxidative phosphorylation were significantly elevated over the Ti disc groups. SiN in aqueous solution releases ammonium/ammonia, which may provide a source for glutamine-dependent energy production. It was confirmed that BM-MSC upregulated the glutamate-ammonia ligase (GLUL) expression with osteogenic condition. In addition, SiN increased the expression of functional gene clusters involving vascular formation. The upregulation of HIF1a in vitro and the increased VEGFR3-positive blanching vascular structures in vivo supported that SiN-induced neovascularization. This study has uncovered an important mechanism that SiN stimulates osteoconduction through unique glutamine-driven mitochondrial oxidative phosphorylation and establishes oxygen and nutrient supply by neovascularization, leading to stable osseointegration.</description><dates><publication>2026/07/01</publication></dates><accession>GSE275703</accession><cross_references><GSM>GSM8483031</GSM><GSM>GSM8483032</GSM><GSM>GSM8483030</GSM><GPL>24676</GPL><GSE>275703</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>