MiR-29 increases apoptosis of retinal ganglion cells in rat glaucoma model through AKT signaling pathway

2021 ◽  
Vol 63 (1) ◽  
Author(s):  
Li YU ◽  
Jie YANG
Keyword(s):  
Signaling Pathway ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Akt Signaling ◽  
Retinal Ganglion ◽  
Akt Signaling Pathway

scholarly journals Downregulation of microRNA-149 in retinal ganglion cells suppresses apoptosis through activation of the PI3K/Akt signaling pathway in mice with glaucoma

2018 ◽  
Vol 315 (6) ◽  
pp. C839-C849 ◽  
Author(s):  
Xin-Gang Nie ◽  
Dong-Sheng Fan ◽  
Yan-Xia Huang ◽  
Ying-Ying He ◽  
Bo-Li Dong ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Akt Signaling ◽  
Luciferase Reporter ◽  
Ultrastructural Changes ◽  
Retinal Ganglion ◽  
Akt Signaling Pathway ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Glaucoma represents a major cause of blindness, generally associated with elevated intraocular pressure (EIOP). The aim of the present study was to investigate whether microRNA-149 (miR-149) affects retinal ganglion cells (RGCs) and the underlying mechanism based on a mouse model of chronic glaucoma with EIOP. The successfully modeled mice were administered with mimics or inhibitors of miR-149. Next, the number of RGCs, ultrastructural changes of RGCs, and purity of RGCs in the retinal tissues were detected. Moreover, the RGCs were collected and subsequently treated with 60 mmHg pressure and transfected with a series of plasmids aiding in the regulation of the expression of miR-149 and betacellulin (BTC). The levels of miR-149, BTC, phosphatidylinositol 3-kinase (PI3K), and Akt were subsequently determined. Finally, RGC viability and apoptosis were detected accordingly. Dual luciferase reporter gene assay provided validation, highlighting BTC was indeed a target gene of miR-149. The downregulation of miR-149 is accompanied by an increased number of RGCs and decreased ultrastructural RGC alterations. Additionally, downregulated miR-149 was noted to increase the levels of BTC, PI3K, and Akt in both the retinal tissues and RGCs, whereas the silencing of miR-149 was observed to promote the viability of RGC and inhibit RGC apoptosis. Taken together, the results of the current study provided validation suggesting that the downregulation of miR-149 confers protection to RGCs by means of activating the PI3K/Akt signaling pathway via upregulation of BTC in mice with glaucoma. Evidence presented indicated the promise of miR-149 inhibition as a potential therapeutic strategy for glaucoma treatment.

Palmitic acid triggers cell apoptosis in RGC-5 retinal ganglion cells through the Akt/FoxO1 signaling pathway

2016 ◽  
Vol 32 (2) ◽  
pp. 453-460 ◽  
Author(s):  
Panshi Yan ◽  
Shu Tang ◽  
Haifeng Zhang ◽  
Yuanyuan Guo ◽  
Zhiwen Zeng ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Signaling Pathway ◽  
Retinal Ganglion Cells ◽  
Cell Apoptosis ◽  
Ganglion Cells ◽  
Retinal Ganglion

scholarly journals Long Non-Coding RNA-MALAT1 Mediates Retinal Ganglion Cell Apoptosis Through the PI3K/Akt Signaling Pathway in Rats with Glaucoma

2017 ◽  
Vol 43 (5) ◽  
pp. 2117-2132 ◽  
Author(s):  
Hai-Bo Li ◽  
Qi-Sheng You ◽  
Li-Xin Xu ◽  
Li-Xin Sun ◽  
Aman Shah Abdul Majid ◽  
...  
Keyword(s):  
Ganglion Cell ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
The Other ◽  
Retinal Ganglion ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Lncrna Malat1 ◽  
Long Non Coding Rna

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.

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