ArticleNeurochemical research2016
Effects of High Glucose on Cell Viability and Differentiation in Primary Cultured Schwann Cells: Potential Role of ERK Signaling Pathway.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Lysosome Evanescence Mediates Autophagic Flux Impairment in Glucose Imbalanced Environments.The Kaohsiung journal of medical sciences · 2026Article
- High glucose mediates diabetic peripheral neuropathy by inducing Schwann cells apoptosis through the Dgkh/PKC-α signaling pathway.Acta diabetologica · 2025Article
- Hyperglycemia Modulates mTOR Signaling and Myelin Protein Expression in Schwann Cells.International journal of molecular sciences · 2025Article
- Daphnetin Protects Schwann Cells Against High-Glucose-Induced Oxidative Injury by Modulating the Nuclear Factor Erythroid 2-Related Factor 2/Glutamate-Cysteine Ligase Catalytic Subunit Signaling Pathway.Plants (Basel, Switzerland) · 2024Article
- Unveiling the Role of Schwann Cell Plasticity in the Pathogenesis of Diabetic Peripheral Neuropathy.International journal of molecular sciences · 2024Review
- Diabetic peripheral neuropathy based on Schwann cell injury: mechanisms of cell death regulation and therapeutic perspectives.Frontiers in endocrinology · 2024Review
- Sex-specific adipose tissue's dynamic role in metabolic and inflammatory response following peripheral nerve injury.iScience · 2023Article
- Article
- Schwann cells-derived exosomal miR-21 participates in high glucose regulation of neurite outgrowth.iScience · 2022Article
- Therapeutic effects and mechanisms of N-(9,10-anthraquinone-2-ylcarbonyl) xanthine oxidase inhibitors on hyperuricemia.Frontiers in pharmacology · 2022Article
- Regulatory Effects of Astragaloside IV on Hyperglycemia-Induced Mitophagy in Schwann Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- A microfabricated multi-compartment device for neuron and Schwann cell differentiation.Scientific reports · 2021Article
- Interactions Among Nerve Regeneration, Angiogenesis, and the Immune Response Immediately After Sciatic Nerve Crush Injury in Sprague-Dawley Rats.Frontiers in cellular neuroscience · 2021Article
- CombiningJournal of the Royal Society, Interface · 2020Article
- Peripheral Glial Cells in the Development of Diabetic Neuropathy.Frontiers in neurology · 2018Review
- Schwann cell interactions with axons and microvessels in diabetic neuropathy.Nature reviews. Neurology · 2017Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic peripheral neuropathy (DPN) is one of the most common complications of diabetes mellitus and hyperglycemia is considered to be the major factor in the development and progression of DPN. Because of the contribution of Schwann cells (SCs) to the pathology of DPN, we investigated the effects of high glucose on cell proliferation, apoptosis and differentiation in primary cultured SCs. Cell Counting Kit-8 (CCK-8) assay and Hoechst staining showed that high glucose inhibited SCs proliferation and increased apoptosis ratio in time and concentration dependent manner. Western blot and real-time quantitative PCR analysis revealed that the major myelin proteins and genes expressions including P0, MAG and Krox-20, were downregulated time dependently in SCs exposed to high glucose from 48 to 96 h. To further elucidate the underlying pathogenic mechanisms, we also explored the role of ERK signaling pathway in high glucose induced SC injury, which has been proved to drive demyelination of peripheral nerves. The western blot analysis showed that compared with control group phosphorylation level of ERK was increased by 14.3 % in SCs exposed to high glucose for 72 h (P < 0.01). Using immunocytochemistry analysis, we observed that the ERK specific inhibitor U0126 blocked the ERK activation induced by high glucose and reversed the inhibitory effect of high glucose on P0 expression. Taken together, these results suggest that high glucose can cause damage in primary cultured SCs and may exert the inhibitory effect on SC differentiation and myelination through ERK signaling activation.
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