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被撤回的出版物: 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RNA-MALAT1 Mediates Retinal Ganglion Cell Apoptosis Through the PI3K/Akt Signaling Pathway in Rats with Glaucoma (Retracted article See vol 55, pg 383, 2021)

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机构: [1]Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, [2]Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, [3]The First People’s Hospital of Changde, Changde, China [4]Department of Pharmacology, Quest International University Perak, Ipoh, Malaysia
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关键词: Long non-coding RNA-MALAT1 PI3K/Akt signaling pathway Glaucoma Retinal ganglion cells Apoptosis

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

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基金编号: 81400442

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出版当年[2016]版:
大类 | 2 区 生物
小类 | 2 区 生理学 3 区 细胞生物学
最新[2025]版:
大类 | 4 区 生物学
小类 | 4 区 细胞生物学 4 区 生理学
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出版当年[2015]版:
Q1 PHYSIOLOGY Q2 CELL BIOLOGY
最新[2024]版:
Q3 PHYSIOLOGY Q4 CELL BIOLOGY

影响因子: 最新[2024版] 最新五年平均 出版当年[2015版] 出版当年五年平均 出版前一年[2014版] 出版后一年[2016版]

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第一作者机构: [1]Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha,
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通讯机构: [1]Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, [3]The First People’s Hospital of Changde, Changde, China [*1]Department of Ophthalmology, Xiangya Hospital, Central South University No. 87, Xiangya Road, Changsha, Hunan Province (China)
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