<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pandya CD</submitter><funding>NCATS NIH HHS</funding><funding>University of Kentucky</funding><funding>NINDS NIH HHS</funding><funding>National Institutes of Health</funding><pagination>13-23</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8016702</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>231</volume><pubmed_abstract>Oligodendrocyte progenitor cells (OPCs) in the infant brain give rise to mature oligodendrocytes that myelinate CNS axons. OPCs are particularly vulnerable to oxidative stress that occurs in many forms of brain injury. One common cause of infant brain injury is neonatal intraventricular hemorrhage (IVH), which releases blood into the CSF and brain parenchyma of preterm infants. Although blood contains the powerful oxidant hemoglobin, the direct effects of hemoglobin on OPCs have not been studied. We utilized a cell culture system to test if hemoglobin induced free radical production and mitochondrial dysfunction in OPCs. We also tested if phenelzine (PLZ), an FDA-approved antioxidant drug, could protect OPCs from hemoglobin-induced oxidative stress. OPCs were isolated from Sprague Dawley r</pubmed_abstract><journal>Translational research : the journal of laboratory and clinical medicine</journal><pubmed_title>Hemoglobin induces oxidative stress and mitochondrial dysfunction in oligodendrocyte progenitor cells.</pubmed_title><pmcid>PMC8016702</pmcid><funding_grant_id>UL1 TR001998</funding_grant_id><funding_grant_id>KL2 TR001996</funding_grant_id><funding_grant_id>K08 NS112580</funding_grant_id><pubmed_authors>Vekaria H</pubmed_authors><pubmed_authors>Gensel JC</pubmed_authors><pubmed_authors>Miller BA</pubmed_authors><pubmed_authors>Slone SA</pubmed_authors><pubmed_authors>Joseph B</pubmed_authors><pubmed_authors>Sullivan PG</pubmed_authors><pubmed_authors>Pandya CD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hemoglobin induces oxidative stress and mitochondrial dysfunction in oligodendrocyte progenitor cells.</name><description>Oligodendrocyte progenitor cells (OPCs) in the infant brain give rise to mature oligodendrocytes that myelinate CNS axons. OPCs are particularly vulnerable to oxidative stress that occurs in many forms of brain injury. One common cause of infant brain injury is neonatal intraventricular hemorrhage (IVH), which releases blood into the CSF and brain parenchyma of preterm infants. Although blood contains the powerful oxidant hemoglobin, the direct effects of hemoglobin on OPCs have not been studied. We utilized a cell culture system to test if hemoglobin induced free radical production and mitochondrial dysfunction in OPCs. We also tested if phenelzine (PLZ), an FDA-approved antioxidant drug, could protect OPCs from hemoglobin-induced oxidative stress. OPCs were isolated from Sprague Dawley r</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2025-04-04T10:15:51.726Z</modification><creation>2025-04-04T10:15:51.726Z</creation></dates><accession>S-EPMC8016702</accession><cross_references><pubmed>33460824</pubmed><doi>10.1016/j.trsl.2021.01.005</doi></cross_references></HashMap>