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MEG3 is involved in the development of glaucoma through promoting the autophagy of retinal ganglion cells

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机构: [1]GuangDong Women & Children Hosp, Dept Ophtalmol, Guangzhou, Guangdong, Peoples R China [2]GuangZhou Medcial Univ, Affiliated Hosp 1, Dept Anesthesiol, Guangzhou, Guangdong, Peoples R China [3]GuangDong Women & Children Hosp, Dept Lab, Guangzhou, Guangdong, Peoples R China [4]Hebei Med Univ, Hosp 4, Dept Ophthalmol, Shijiazhuang, Hebei, Peoples R China [5]Guangdong Med Univ, Affiliated Hosp, Dept Oncol, Zhanjiang, Peoples R China
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关键词: Glaucoma Ocular hypertension MEG3 Autophagy Apoptosis

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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 qRTPCR 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 MEGS 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.

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大类 | 4 区 医学
小类 | 4 区 药学
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Q2 PHARMACOLOGY & PHARMACY
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第一作者机构: [1]GuangDong Women & Children Hosp, Dept Ophtalmol, Guangzhou, Guangdong, Peoples R China
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