RETRACTED: Long Non-Coding RNA-MALAT1 Mediates Retinal Ganglion Cell Apoptosis Through the PI3K/Akt Signaling Pathway in Rats with Glaucoma (Retracted article. See vol. 55, pg. 383, 2021)

被引:49
作者
Li, Hai-Bo [1 ]
You, Qi-Sheng [2 ]
Xu, Li-Xin [3 ]
Sun, Li-Xin [3 ]
Majid, Aman Shah Abdul [4 ]
Xia, Xiao-Bo [1 ]
Ji, Dan [1 ,3 ]
机构
[1] Cent South Univ, Xiangya Hosp, Dept Ophthalmol, 87 Xiangya Rd, Changsha, Hunan, Peoples R China
[2] Capital Med Univ, Beijing Tongren Hosp, Beijing Tongren Eye Ctr, Beijing Inst Ophthalmol, Beijing, Peoples R China
[3] First Peoples Hosp Changde, Changde, Peoples R China
[4] Quest Int Univ Perak, Dept Pharmacol, Ipoh, Malaysia
基金
中国国家自然科学基金;
关键词
Long non-coding RNA-MALAT1; PI3K/Akt signaling pathway; Glaucoma; Retinal ganglion cells; Apoptosis; VISUAL-FIELD LOSS; INTRAOCULAR-PRESSURE; STEM-CELLS; ACTIVATION; RNA; SURVIVAL; MALAT1; PROLIFERATION; CONTRIBUTES; METASTASIS;
D O I
10.1159/000484231
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: The aim of the present study is to investigate the effect of long non-coding RNA-MALAT1 (LncRNA-MALAT1) on retinal ganglion cell (RGC) apoptosis mediated by the PI3K/Akt signaling pathway in rats with glaucoma. Methods: RGCs were isolated and cultured, and monoclonal antibodies (anti-rat Thy-1, Brn3a and RBPMS) were examined by immunocytochemistry. An overexpression vector MALAT1-RNA activation (RNAa), gene knockout vector MALAT1-RNA interference (RNAi), and control vector MALAT1-negative control (NC) were constructed. A chronic high intraocular pressure (IOP) rat model of glaucoma was established by episcleral vein cauterization. The RGCs were divided into the RGC control, RGC pressure, RGC pressure + MALAT1-NC, RGC pressure + MALAT1-RNAi and RGC pressure + MALAT1-RNAa groups. Sixty Sprague-Dawley (SD) rats were randomly divided into the normal, high IOP, high IOP + MALAT1-NC, high IOP + MALAT1-RNAa and high IOP + MALAT1-RNAi groups. qRT-PCR and western blotting were used to detect the expression levels of LncRNA-MALAT1 and PI3K/Akt. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and flow cytometry were used to detect RGC apoptosis. Results: Immunocytochemistry revealed that the cultured RGCs reached 90% purity. Compared with the RGC pressure + MALAT1-NC group, the RGC pressure + MALAT1-RNAa group exhibited elevated expression levels of MALAT1, lower total protein levels of PI3K and Akt and decreased RGC apoptosis, while these expression levels were reversed in the RGC pressure + MALAT1-RNAi group. RGC numbers and PI3K/Akt expression levels in the high IOP model groups were lower than those in the normal group. In the high IOP + MALAT1-RNAa group, the mRNA and protein expression levels of PI3K/Akt were reduced but higher than those in the other three high IOP model groups. Additionally, RGC numbers in the high IOP + MALAT1-RNAa group were lower than those in the normal group but higher than those in the other three high IOP model groups. Conclusion: Our study provides evidence that LncRNA-MALAT1 could inhibit RGC apoptosis in glaucoma through activation of the PI3K/Akt signaling pathway. (c) 2017 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:2117 / 2132
页数:16
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