{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338573/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338573"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"DPSCs Transfer Mitochondria via TNTs to Drive Hypoxic Angiogenesis","description":"The dental pulp resides within a rigid dentin chamber with a limited blood supply, creating a hypoxic environment that impedes tissue regeneration. This study identifies intercellular mitochondrial transfer as a critical endogenous rescue mechanism. Human dental pulp stem cells (DPSCs) actively transfer functional mitochondria to green fluorescent protein-expressing human umbilical vein endothelial cells (GFP-ECs) under hypoxic stress. This transfer significantly reduces hypoxia-induced apoptosis, preserves mitochondrial membrane potential, and enhances the angiogenic capacities of recipient ECs. To uncover the molecular mechanisms driving this phenotype, RNA-sequencing (RNA-seq) was performed on mitochondrial-transferred ECs (Mito(+)) and control ECs (Mito(-)) under hypoxia.","dates":{"publication":"2026/07/15"},"accession":"GSE338573","cross_references":{"GSM":["GSM9877639","GSM9877635","GSM9877636","GSM9877637","GSM9877638","GSM9877640"],"GPL":["24676"],"GSE":["338573"],"taxon":["Homo sapiens"]}}