OBJECTIVE: In this study, we aimed at investigating whether MEG3 may be involved in the pathogenesis of glaucoma by regulating the autophagy of retinal ganglion cells (RGCs).
MATERIALS AND METHODS: We used qRT-PCR to detect the expression of MEG3 in RGC-5s cell line under high hydrostatic pressure. RGC-5s were transfected with a lentiviral vector to achieve MEG3 overexpression or knockdown. The influence of overexpression or inhibition of MEG3 on cell proliferation and apoptosis was observed using CCK-8 test and flow cytometry. After overexpression of MEG3 and/or knockdown of MEG3 or Beclin-1, detection of the expressions of autophagy-related and apoptosis-related proteins was performed using Western blot.
RESULTS: MEG3 expression level increased in RGC-5 cells under high hydrostatic pressure, while exogenously decreased MEG3 expression can reverse the impact of the high pressure on RGC-5 cells. Additionally, overexpression of MEG3 can improve Atg3 expression, promote cell apoptosis, inhibit cell proliferation, and enhance autophagy levels. Meanwhile, knockdown of Beclin-1 up-regulated Bcl-2 level.
CONCLUSIONS: Upregulation of MEG3 is involved in the pathogenesis of glaucoma through promoting apoptosis of retinal ganglion cells, the mechanism of which may be related to the enhanced autophagy levels.Free PDF Download
To cite this article
W. Sun, Y.-N. Li, J.-F. Ye, Y.-Q. Guan, S.-J. Li
MEG3 is involved in the development of glaucoma through promoting the autophagy of retinal ganglion cells
Eur Rev Med Pharmacol Sci
Vol. 22 - N. 9