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RNA-MALAT1 Mediates Retinal Ganglion Cell Apoptosis Through the PI3K/Akt Signaling Pathway in Rats with Glaucoma (Retracted article See vol 55, pg 383, 2021)
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,研究所眼科研究所首都医科大学附属北京同仁医院首都医科大学附属同仁医院[3]The First People’s Hospital of Changde, Changde, China[4]Department of Pharmacology, Quest International University Perak, Ipoh, Malaysia
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
基金:
National Natural Science Foundation of China (NSFC) [81400442]
第一作者机构:[1]Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha,
共同第一作者:
通讯作者:
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)
推荐引用方式(GB/T 7714):
Li Hai-Bo,You Qi-Sheng,Xu Li-Xin,et al.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)[J].CELLULAR PHYSIOLOGY AND BIOCHEMISTRY.2017,43(5):2117-2132.doi:10.1159/000484231.
APA:
Li, Hai-Bo,You, Qi-Sheng,Xu, Li-Xin,Sun, Li-Xin,Majid, Aman Shah Abdul...&Ji, Dan.(2017).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).CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,43,(5)
MLA:
Li, Hai-Bo,et al."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)".CELLULAR PHYSIOLOGY AND BIOCHEMISTRY 43..5(2017):2117-2132