Inhibition of miRNA-21 promotes retinal ganglion cell survival and visual function by modulating Muller cell gliosis after optic nerve crush
Inhibition of miRNA-21 promotes retinal ganglion cell survival and visual function by modulating Muller cell gliosis after optic nerve crush
复制标题
抑制 miRNA-21 通过调节视神经挤压后 Muller 细胞胶质增生促进视网膜神经节细胞存活和视觉功能
DOI：
10.1016/j.yexcr.2019.01.009
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发表时间：
2019-02-15
影响因子：
3.7
通讯作者：
Feng, Dong-Fu
中科院分区：
文献类型：
--
作者：
Li, Hong-Jiang;Sun, Zhao-Liang;Feng, Dong-Fu
Background: Muller cell gliosis not only plays an important physiological role by maintaining retinal neuronal homeostasis but is also associated with multiple pathological events in the retina, including optic nerve crush (ONC) injury. Modulating Muller cell gliosis contributes to the creation of a permissive environment for neuronal survival. However, the underlying mechanism of Muller cell gliosis has remained elusive.Objective: To investigate the underlying mechanism of Miller cell gliosis after ONC.Methods: Rats with ONC injury were transfected with miRNA-21 (miR-21) agomir (overexpressing miR-21) or antagomir (inhibiting miR-21) via intravitreous injection. Immunofluorescence and western blotting were performed to confirm the effects of miR-21 on Muller cell gliosis. The retinal nerve fiber layer (RNFL) thickness was measured using optical coherence tomography and the positive scotopic threshold response (pSTR) was recorded using electroretinogram.Results: In the acute phase (14 days) after ONC, compared with the crushed group, inhibiting miR-21 promoted Muller cell gliosis, exhibiting thicker processes and increased GFAP expression. In the chronic phase (35 days), inhibiting miR-21 ameliorated Muller cell gliosis, which exhibited thicker and denser processes and increased GFAP expression. Retinal ganglion cell (RGC) counts in retinas showed that the number of surviving RGCs increased significantly in the antagomir group. The thickness of the RNFL increased significantly, and pSTR showed significant preservation of the amplitudes in the antagomir group.Conclusions: Inhibition of miR-21 promotes RGC survival, RNFL thickness and the recovery of RGC function by modulating Muller cell gliosis after ONC.
