<HashMap><database>biostudies-literature</database><scores/><additional><submitter>D'Souza A</submitter><funding>NCI NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>505-526</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8526414</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>338</volume><pubmed_abstract>We have demonstrated, for the first time that microvesicles, a sub-type of extracellular vesicles (EVs) derived from hCMEC/D3: a human brain endothelial cell (BEC) line transfer polarized mitochondria to recipient BECs in culture and to neurons in mice acute brain cortical and hippocampal slices. This mitochondrial transfer increased ATP levels by 100 to 200-fold (relative to untreated cells) in the recipient BECs exposed to oxygen-glucose deprivation, an in vitro model of cerebral ischemia. We have also demonstrated that transfer of microvesicles, the larger EV fraction, but not exosomes resulted in increased mitochondrial function in hypoxic endothelial cultures. Gene ontology and pathway enrichment analysis of EVs revealed a very high association to glycolysis-related processes. In comp</pubmed_abstract><journal>Journal of controlled release : official journal of the Controlled Release Society</journal><pubmed_title>Microvesicles transfer mitochondria and increase mitochondrial function in brain endothelial cells.</pubmed_title><pmcid>PMC8526414</pmcid><funding_grant_id>P30 CA047904</funding_grant_id><funding_grant_id>R25 NS100118</funding_grant_id><funding_grant_id>T32 GM007635</funding_grant_id><pubmed_authors>Reynolds MJ</pubmed_authors><pubmed_authors>Shiva SS</pubmed_authors><pubmed_authors>Dobbins DX</pubmed_authors><pubmed_authors>Quillinan N</pubmed_authors><pubmed_authors>Sabatelle C</pubmed_authors><pubmed_authors>Manickam DS</pubmed_authors><pubmed_authors>Zhao W</pubmed_authors><pubmed_authors>Joy GM</pubmed_authors><pubmed_authors>Soman V</pubmed_authors><pubmed_authors>D'Souza A</pubmed_authors><pubmed_authors>Dave KM</pubmed_authors><pubmed_authors>Herson PS</pubmed_authors><pubmed_authors>Chandran UR</pubmed_authors><pubmed_authors>Burch A</pubmed_authors><pubmed_authors>Kamte YS</pubmed_authors><pubmed_authors>Sreeram A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Microvesicles transfer mitochondria and increase mitochondrial function in brain endothelial cells.</name><description>We have demonstrated, for the first time that microvesicles, a sub-type of extracellular vesicles (EVs) derived from hCMEC/D3: a human brain endothelial cell (BEC) line transfer polarized mitochondria to recipient BECs in culture and to neurons in mice acute brain cortical and hippocampal slices. This mitochondrial transfer increased ATP levels by 100 to 200-fold (relative to untreated cells) in the recipient BECs exposed to oxygen-glucose deprivation, an in vitro model of cerebral ischemia. We have also demonstrated that transfer of microvesicles, the larger EV fraction, but not exosomes resulted in increased mitochondrial function in hypoxic endothelial cultures. Gene ontology and pathway enrichment analysis of EVs revealed a very high association to glycolysis-related processes. In comp</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-06-01T02:11:10.914Z</modification><creation>2025-02-19T01:27:48.084Z</creation></dates><accession>S-EPMC8526414</accession><cross_references><pubmed>34450196</pubmed><doi>10.1016/j.jconrel.2021.08.038</doi></cross_references></HashMap>