ArticlePloS one2011
A role for hemopexin in oligodendrocyte differentiation and myelin formation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Matrix metalloprotease-9 modulates microglial/macrophage responses in murine brain demyelination.Acta neuropathologica communications · 2026Article
- The association of hemopexin, muscle quality, and sarcopenia in Japanese older adults with cognitive impairment: a cross-sectional study.BMC geriatrics · 2025Article
- Rnd3 is necessary for the correct oligodendrocyte differentiation and myelination in the central nervous system.Brain structure & function · 2022Article
- Skeletal muscle atrophy-induced hemopexin accelerates onset of cognitive impairment in Alzheimer's disease.Journal of cachexia, sarcopenia and muscle · 2021Article
- What Is Next in This "Age" of Heme-Driven Pathology and Protection by Hemopexin? An Update and Links with Iron.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Mitochondrial Targeting in Neurodegeneration: A Heme Perspective.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Hemopexin is required for adult neurogenesis in the subventricular zone/olfactory bulb pathway.Cell death & disease · 2018Article
- Plasma Hemopexin ameliorates murine spinal cord injury by switching microglia from the M1 state to the M2 state.Cell death & disease · 2018Article
- Metformin Attenuates Cognitive Impairments in Hypoxia-Ischemia Neonatal Rats via Improving Remyelination.Cellular and molecular neurobiology · 2017Article
- Subventricular zone involvement in Glioblastoma - A proteomic evaluation and clinicoradiological correlation.Scientific reports · 2017Article
- Alterations in Systemic Extracellular Heme and Hemopexin Are Associated With Adverse Clinical Outcomes in Ugandan Children With Severe Malaria.The Journal of infectious diseases · 2016Article
- Deletion of the hemopexin or heme oxygenase-2 gene aggravates brain injury following stroma-free hemoglobin-induced intracerebral hemorrhage.Journal of neuroinflammation · 2016Article
- Hemopexin and haptoglobin: allies against heme toxicity from hemoglobin not contenders.Frontiers in physiology · 2015Review
- Discovery and characterization of potential prognostic biomarkers for dengue hemorrhagic fever.The American journal of tropical medicine and hygiene · 2014Article
- Hemoglobin as a source of iron overload in multiple sclerosis: does multiple sclerosis share risk factors with vascular disorders?Cellular and molecular life sciences : CMLS · 2014Article
- FGF8 activates proliferation and migration in mouse post-natal oligodendrocyte progenitor cells.PloS one · 2014Article
- Heme in pathophysiology: a matter of scavenging, metabolism and trafficking across cell membranes.Frontiers in pharmacology · 2014Review
- The MMP-9/TIMP-1 axis controls the status of differentiation and function of myelin-forming Schwann cells in nerve regeneration.PloS one · 2012Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin formation and maintenance are crucial for the proper function of the CNS and are orchestrated by a plethora of factors including growth factors, extracellular matrix components, metalloproteases and protease inhibitors. Hemopexin (Hx) is a plasma protein with high heme binding affinity, which is also locally produced in the CNS by ependymal cells, neurons and glial cells. We have recently reported that oligodendrocytes (OLs) are the type of cells in the brain that are most susceptible to lack of Hx, as the number of iron-overloaded OLs increases in Hx-null brain, leading to oxidative tissue damage. In the current study, we found that the expression of the Myelin Basic Protein along with the density of myelinated fibers in the basal ganglia and in the motor and somatosensory cortex of Hx-null mice were strongly reduced starting at 2 months and progressively decreased with age. Myelin abnormalities were confirmed by electron microscopy and, at the functional level, resulted in the inability of Hx-null mice to perform efficiently on the Rotarod. It is likely that the poor myelination in the brain of Hx-null mice was a consequence of defective maturation of OLs as we demonstrated that the number of mature OLs was significantly reduced in mutant mice whereas that of precursor cells was normal. Finally, in vitro experiments showed that Hx promotes OL differentiation. Thus, Hx may be considered a novel OL differentiation factor and the modulation of its expression in CNS may be an important factor in the pathogenesis of human neurodegenerative disorders.
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