ArticleMolecular medicine reports2019
Effects of the transcription factor Olig1 on the differentiation and remyelination of oligodendrocyte precursor cells after focal cerebral ischemia in rats.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 15 citations in OpenAlex.
- Neuroimmune-oligovascular signaling shapes oligodendrocyte precursor cell fate and repair after ischemic stroke.Cell communication and signaling : CCS · 2026Review
- Sex-specific lateralization of the effects of exogenously-induced neuroimmune activation in the amygdala on pain-like behaviors.Frontiers in pharmacology · 2026Article
- Breast milk stem cells integrate into cellular remodeling and functional differentiation in the ischemic brain.Scientific reports · 2025Article
- p39 Affects Myelin Formation in Cerebral Ischemic Injury.Neuromolecular medicine · 2024Article
- Ibogaine administration following repeated morphine administration upregulates myelination markers 2', 3'-cyclic nucleotide 3'-phosphodiesterase (CNP) and myelin basic protein (MBP) mRNA and protein expression in the internal capsule of Sprague Dawley rats.Frontiers in neuroscience · 2024Article
- Anti-inflammatory mechanisms and pharmacological actions of phycocyanobilin in a mouse model of experimental autoimmune encephalomyelitis: A therapeutic promise for multiple sclerosis.Frontiers in immunology · 2022Article
- NEP1‑40 promotes myelin regeneration via upregulation of GAP‑43 and MAP‑2 expression after focal cerebral ischemia in rats.Molecular medicine reports · 2021Article
- Knockdown of G protein-coupled receptor-17 (GPR17) facilitates the regeneration and repair of myelin sheath post-periventricular leukomalacia (PVL).Bioengineered · 2021Article
- Remyelination in PNS and CNS: current and upcoming cellular and molecular strategies to treat disabling neuropathies.Molecular biology reports · 2021Review
- The Effects of the Olig Family on the Regulation of Spinal Cord Development and Regeneration.Neurochemical research · 2021Review
- AInternational journal of molecular sciences · 2020Review
- Systematical Identification of the Protective Effect of Danhong Injection and BuChang NaoXinTong Capsules on Transcription Factors in Cerebral Ischemia Mice Brain.Oxidative medicine and cellular longevity · 2020Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The differentiation and maturation of oligodendrocyte precursor cells (OPCs) is important for remyelination in the central nervous system. Nevertheless, this process is often limited and incomplete in ischemic injury. Oligodendrocyte transcription factor 1 (Olig1) is important for the maturation of OPCs and the repair of demyelinated lesions. However, how Olig1 modulates the development of OPCs or the remyelination associated with ischemic injury remains unclear. The present study aimed to examine alterations in OPCs, and the expression of myelin and Olig1, at different time-points after focal cerebral ischemia using immunohistochemistry and western blot techniques to elucidate the role of Olig1 in the maturation of OPCs and remyelination. The present results showed that the expression of Olig1 significantly decreased at 1 day after middle cerebral artery occlusion (MCAO) and returned to normal levels from day 3 to 28. Additionally, Olig1 was found to translocate into the nucleus following ischemia in the brain. The number of OPCs in the ischemic striatum significantly declined at days 1 and 3 following MCAO, and increased at days 7, 14 and 28 compared with the control. The expression of myelin basic protein, a marker of mature oligodendrocytes and myelin, gradually decreased from day 1 to 7 after ischemia and recovered at day 14 and 28; however, the levels were lower than those in the control group. The present results indicated that the restored normal level of Olig1 following ischemia may play an important role in the maturation of OPCs through its translocation into the nucleus, where it may promote the growth and development of myelin under pathological conditions. However, this endogenous recovery mechanism fails to fully repair the demyelinated lesion. The data of the present study may help clinicians understand the expression pattern of Olig1 and its potential role in endogenous remyelination after ischemia, which may have implications for the treatment of diseases that lead to demyelination.
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