ArticleInternational journal of clinical and experimental pathology2015
EPO protects Müller cell under high glucose state through BDNF/TrkB pathway.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Mechanisms of Erythropoietin-Mediated Protection Against Retinal Ganglion Cell Apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- Salidroside protects RGC from pyroptosis in diabetes-induced retinopathy associated with NLRP3, NFEZL2 and NGKB1, revealed by network pharmacology analysis and experimental validation.European journal of medical research · 2024Article
- Three Major Causes of Metabolic Retinal Degenerations and Three Ways to Avoid Them.International journal of molecular sciences · 2023Review
- Apocynin ameliorates NADPH oxidase 4 (NOX4) induced oxidative damage in the hypoxic human retinal Müller cells and diabetic rat retina.Molecular and cellular biochemistry · 2021Article
- An Update on Connexin Gap Junction and Hemichannels in Diabetic Retinopathy.International journal of molecular sciences · 2021Review
- Relevance of Peptide Homeostasis in Metabolic Retinal Degenerative Disorders: Curative Potential in Genetically Modified Mice.Frontiers in pharmacology · 2021Review
- Mechanisms behind Retinal Ganglion Cell Loss in Diabetes and Therapeutic Approach.International journal of molecular sciences · 2020Review
- Neuroprotection Strategies for Term Encephalopathy.Seminars in pediatric neurology · 2019Review
- Human Mesenchymal Stem Cells Expressing Erythropoietin Enhance Survivability of Retinal Neurons Against Oxidative Stress: AnFrontiers in cellular neuroscience · 2018Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotrophic factor decreased in the early stage of diabetic retinal nerve cells. Neurons damage brain derived neurotrophic factor (BDNF) and receptor TrkB expression reduced. Erythropoietin (EPO) plays an important role in protecting early diabetic retinopathy. The rats were euthanized at 24 h after EPO vitreous injection and the retina was separated. HE staining was applied to observe the pathological tissue morphology. Immunohistochemistry, immunofluorescence, and Western blot were used to detect BDNF, TrkB, extracellular signal-regulated kinase (ERK), and glial fibrillary acidic portein (GFAP) expression. Retinal structure was clear in group C, while the retinal thickness and RGCs number decreased in group B at 24 w. Retinal thickness in group E was greater than in group B but lower than in group C. GFAP and ERK expression increased in both group B and E, whereas the latter was significantly lower than the former. TrkB protein level was in group E > B > C at 4 w, while it was in group C > group E > group B at 24 w. BDNF expression in group B was higher than in group C at 4 w, whereas it was opposite at 24 w. BDNF expression increased in group E at 4 w, and it was similar in group E compared with group C at 24 w. EPO vitreous injection can increase BDNF and TrkB expression, while reduce GFAP and ERK expression in diabetes rat retina. It could protect Müller cells through BDNF/TrkB pathway to play a role of nerve nutrition.
Indexed as
Identifiers
26339375PMC4555703W1232582588What OpenQuestion holds
Registered trials
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