ArticleTranslational research : the journal of laboratory and clinical medicine2021
Hemoglobin induces oxidative stress and mitochondrial dysfunction in oligodendrocyte progenitor cells.
Article in Translational research : the journal of laboratory and clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Erythrocyte Fragility in Progressive Multiple Sclerosis.European journal of neurology · 2026Article
- Acellular Hemoglobin Impairs Cardiomyocyte Excitation-Contraction Coupling.ASAIO journal (American Society for Artificial Internal Organs : 1992) · 2026Article
- Newcastle disease virus hijacks chicken red blood cells as dissemination vehicles with concomitant adsorption-mediated cell death.Veterinary research · 2025Article
- Developmental stage-dependent transcriptomic responses to neonatal intraventricular hemorrhage.Journal of neuroinflammation · 2025Article
- Untargeted Metabolomics-Based Characterization of the Metabolic Profile and Antioxidant Activity ofJournal of fungi (Basel, Switzerland) · 2025Article
- Sex- and Tissue-Specific Effects of Leukemia Inhibitory Factor on Mitochondrial Bioenergetics Following Ischemic Stroke.Biomolecules · 2025Article
- Pro-Oxidative and Inflammatory Actions of Extracellular Hemoglobin and Heme: Molecular Events and Implications for Alzheimer's and Parkinson Disease.Biomolecules & therapeutics · 2025Review
- Metabolomics and Transcriptomics Reveal the Effects of Different Fermentation Times on Antioxidant Activities ofJournal of fungi (Basel, Switzerland) · 2025Article
- Major heme proteins hemoglobin and myoglobin with respect to their roles in oxidative stress - a brief review.Frontiers in chemistry · 2025Review
- Article
- Myelin Pathology in Alzheimer's Disease: Potential Therapeutic Opportunities.Aging and disease · 2024Review
- Azithromycin reduces hemoglobin-induced innate neuroimmune activation.Experimental neurology · 2024Article
- Germinal matrix hemorrhage induces immune responses, brain injury, and motor impairment in neonatal rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Innate immune activation and white matter injury in a rat model of neonatal intraventricular hemorrhage are dependent on developmental stage.Experimental neurology · 2023Article
- Review
- Antenatal and Postnatal Sequelae of Oxidative Stress in Preterm Infants: A Narrative Review Targeting Pathophysiological Mechanisms.Antioxidants (Basel, Switzerland) · 2023Review
- Innate immune activation and white matter injury in a rat model of neonatal intraventricular hemorrhage are dependent on developmental stage.Research square · 2023Article
- Ferroptosis: Underlying mechanism and the crosstalk with other modes of neuronal death after intracerebral hemorrhage.Frontiers in cellular neuroscience · 2023Review
- Extracellular Hemoglobin: Modulation of Cellular Functions and Pathophysiological Effects.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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 rat pups and exposed to hemoglobin with and without PLZ. Outcomes assessed included intracellular reactive oxygen species levels using 2',7'-dichlorodihydrofluorescein diacetate (DCF-DA) fluorescent dye, oxygen consumption using the XFe96 Seahorse assay, and proliferation measured by BrdU incorporation assay. Hemoglobin induced oxidative stress and impaired mitochondrial function in OPCs. PLZ treatment reduced hemoglobin-induced oxidative stress and improved OPC mitochondrial bioenergetics. The effects of hemoglobin and PLZ on OPC proliferation were not statistically significant, but showed trends towards hemoglobin reducing OPC proliferation and PLZ increasing OPC proliferation (P=0.06 for both effects). Collectively, our results indicate that hemoglobin induces mitochondrial dysfunction in OPCs and that antioxidant therapy reduces these effects. Therefore, antioxidant therapy may hold promise for white matter diseases in which hemoglobin plays a role, such as neonatal IVH.
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