微小RNA-100的下调可保护视网膜神经节细胞凋亡并促进其神经元生长。
Downregulation of microRNA-100 protects apoptosis and promotes neuronal growth in retinal ganglion cells.
作者信息
Kong Ning, Lu Xiaohe, Li Bin
机构信息
Department of Ophthalmology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, Guangdong Province, China.
Department of Ophthalmology, Guangzhou Panyu Central Hospital, Guangzhou, 510280, Guangdong Province, China.
出版信息
BMC Mol Biol. 2014 Nov 18;15:25. doi: 10.1186/s12867-014-0025-1.
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 H2O2 was added to induce oxidative stress. TUNEL assay and qRT-PCR showed H2O2 induced apoptosis and up-regulated miR-100 in a dose-dependent manner in RGC-5 cells. Conversely, lentiviral-mediated miR-100 down-regulation protected H2O2 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 H2O2 induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation.
背景
视网膜神经节细胞（RGCs）在青光眼或视神经炎中优先丢失。在本研究中，我们研究了微小RNA 100（miR - 100）对RGC - 5细胞中氧化应激诱导的细胞凋亡的保护作用。
结果
将大鼠RGC - 5细胞培养于培养板中，并加入过氧化氢（H2O2）以诱导氧化应激。TUNEL检测和qRT - PCR显示，H2O2以剂量依赖的方式诱导RGC - 5细胞凋亡并上调miR - 100。相反，慢病毒介导的miR - 100下调可保护细胞免受H2O2诱导的凋亡，促进神经突生长，并通过磷酸化激活AKT/ERK和TrkB信号通路。荧光素酶检测证实，在RGC - 5细胞中IGF1R受miR - 100直接调控，并且siRNA介导的IGF1R敲低通过磷酸化激活AKT蛋白，下调miR - 100，从而对RGC - 5细胞凋亡发挥保护作用。
结论
下调miR - 100是保护RGC - 5细胞免受H2O2诱导凋亡的有效方法，可能与IGF1R调控有关。
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