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Downregulation of microRNA-100 protects apoptosis and promotes neuronal growth in retinal ganglion cells

BACKGROUND: Retinal ganglion cells (RGCs) are preferentially lost in glaucoma or optic neuritis. In the present study, we investigated the protective effect of mircoRNA 100 (miR-100) against oxidative stress induced apoptosis in RGC-5 cells. RESULTS: Rat RGC-5 cells were cultured in plates and H(2)O...

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Detalles Bibliográficos
Autores principales: Kong, Ning, Lu, Xiaohe, Li, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271342/
https://www.ncbi.nlm.nih.gov/pubmed/25406880
http://dx.doi.org/10.1186/s12867-014-0025-1
Descripción
Sumario:BACKGROUND: Retinal ganglion cells (RGCs) are preferentially lost in glaucoma or optic neuritis. In the present study, we investigated the protective effect of mircoRNA 100 (miR-100) against oxidative stress induced apoptosis in RGC-5 cells. RESULTS: Rat RGC-5 cells were cultured in plates and H(2)O(2) was added to induce oxidative stress. TUNEL assay and qRT-PCR showed H(2)O(2) induced apoptosis and up-regulated miR-100 in a dose-dependent manner in RGC-5 cells. Conversely, lentiviral-mediated miR-100 down-regulation protected H(2)O(2) induced apoptosis, promoted neurite growth and activated AKT/ERK and TrkB pathways through phosphorylation. Luciferase assay confirmed that IGF1R was directly regulated by miR-100 in RGC-5 cells, and siRNA-mediated IGF1R knockdown activated AKT protein through phosphorylation, down-regulated miR-100, therefore exerted a protective effect on RGC-5 apoptosis. CONCLUSION: Down-regulating miR-100 is an effective method to protect H(2)O(2) induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation.