Downregulation of microRNA-100 protects apoptosis and promotes neuronal growth in retinal ganglion cells
BMC Molecular Biology, ISSN: 1471-2199, Vol: 15, Issue: 1, Page: 25
2014
- 41Citations
- 29Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations41
- Citation Indexes41
- 41
- CrossRef29
- Captures29
- Readers29
- 29
Article Description
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 HO was added to induce oxidative stress. TUNEL assay and qRT-PCR showed HO induced apoptosis and up-regulated miR-100 in a dose-dependent manner in RGC-5 cells. Conversely, lentiviral-mediated miR-100 down-regulation protected HO 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 HO induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation.
Bibliographic Details
Springer Science and Business Media LLC
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