ArticleMedical science monitor : international medical journal of experimental and clinical research2025
Mechanisms of Erythropoietin-Mediated Protection Against Retinal Ganglion Cell Apoptosis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Targeting Sensory Neuropathies Through Neurotrophin-Based Approaches.Cellular and molecular neurobiology · 2026Review
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4 authors.
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Abstract
BACKGROUND Retinal ganglion cells (RGCs), as cells located in the innermost layer of the retina, are the last cells in the eye neural network to receive visual stimuli. This study aimed to investigate the effects of erythropoietin (EPO) on apoptosis of RGCs and clarify the mechanisms. MATERIAL AND METHODS RGCs were isolated from the mice retinas, purified with the immunopanning method, and identified by immunohistochemical assay. EPO-overexpressed lentivirus (Ov-EPO) was constructed and infected to RGCs. CCK-8 assay and TUNEL assay were used to determine RGC viability and apoptosis, respectively. RT-qPCR assay was applied to detect transcriptions of the Bcl-2, AKT1, STAT5A, and MAPK genes in RGCs treated with Ov-EPO and/or H₂O₂/NMDA. RESULTS Ov-EPO lentivirus was successfully established, showing higher expressing efficacy. TUNEL findings showed that EPO overexpression inhibited apoptosis of RGCs. EPO overexpression resisted oxidative damage, and excitatory toxicity caused cell death. EPO overexpression significantly increased the transcription of the AKT1 and STAT5A gene, compared with those of the blank group, suggesting activated PI3K/Akt and JAK/STAT signaling pathway in RGCs. The transcription of the MAPK gene in EPO-overexpressed RGCs was significantly increased compared with that of the RGCs of the blank group (P<0.01), suggesting that EPO overexpression is associated with the MAPK/ERK signaling pathway. CONCLUSIONS EPO played a protective role for RGC viability, and Bcl-2 played a critical role in this process. EPO inhibited apoptosis, oxidative damage, and excitatory toxicity of RGCs, which involved the potential PI3K/Akt-JAK/STAT-MAPK/ERK signaling pathway.
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