ArticleNeurochemical research2015
Erythropoietin attenuates advanced glycation endproducts-induced toxicity of Schwann cells in vitro.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Immortalized Schwann cell lines as useful tools for pathogenesis-based therapeutic approaches to diabetic peripheral neuropathy.Frontiers in endocrinology · 2024Review
- Review
- Recombinant Erythropoietin Induces Oligodendrocyte Progenitor Cell Proliferation After Traumatic Brain Injury and Delayed Hypoxemia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023Review
- Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System.Biomolecules · 2023Review
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- Advanced Glycation End Products: New Clinical and Molecular Perspectives.International journal of environmental research and public health · 2021Review
- Aldose Reductase and the Polyol Pathway in Schwann Cells: Old and New Problems.International journal of molecular sciences · 2021Review
- New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020Review
- Immunomodulatory Mechanism and Potential Therapies for Perinatal Hypoxic-Ischemic Brain Damage.Frontiers in pharmacology · 2020Review
- Cognitive impairment with diabetes mellitus and metabolic disease: innovative insights with the mechanistic target of rapamycin and circadian clock gene pathways.Expert review of clinical pharmacology · 2020Review
- Dysregulation of metabolic flexibility: The impact of mTOR on autophagy in neurodegenerative disease.International review of neurobiology · 2020Review
- Erythropoietin Protects Against Cognitive Impairment and Hippocampal Neurodegeneration in Diabetic Mice.Behavioral sciences (Basel, Switzerland) · 2018Article
- The mechanistic target of rapamycin (mTOR) and the silent mating-type information regulation 2 homolog 1 (SIRT1): oversight for neurodegenerative disorders.Biochemical Society transactions · 2018Review
- Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors.Current neurovascular research · 2018Review
- Nonenzymatic glycation interferes with fibronectin-integrin interactions in vascular smooth muscle cells.Microcirculation (New York, N.Y. : 1994) · 2017Article
- Glycative Stress and Its Defense Machinery Glyoxalase 1 in Renal Pathogenesis.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation endproducts (AGEs)-induced cytotoxicity is regarded as one of the main mechanisms responsible for neurological disorders. Although erythropoietin (EPO) is demonstrated to have neuroprotective effects in neurodegenerative diseases, the effects of EPO on AGEs-induced toxicity of Schwann cells (SCs) remain open for investigation. Primary cultured SCs isolated from 4 day-old Wistar rats were exposed to AGEs with or without EPO treatment for 5 days. AGEs decreased cell viability, increased apoptotic rate, elevated intracellular reactive oxygen species levels, and reduced total glutathione levels of SCs. The AGEs-induced toxic effects on SCs were partially blocked by AGER siRNA or AGER inhibitor FPS-ZM1. SCs exposed to AGEs exhibited higher mRNA and protein levels of receptor for AGEs (AGER), EPO, and EPO receptor (EPOR). Exogenous EPO treatment attenuated AGEs-induced oxidative stress and apoptosis probably by reducing the mRNA and protein expression of AGER. The protective effect of EPO against AGEs-induced toxicity was blocked by EPOR siRNA. The data of the present study gives, for the first time, evidence of the protective effects of EPO on SCs with AGEs-induced oxidative stress and apoptosis. These results imply that EPO might be a novel valuable agent for treating AGEs-induced toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.