Effects of miR-26a-5p on high glucose-induced retina Müller activation and apoptosis by regulating PTEN/PI3K/Akt signaling pathway
- VernacularTitle:miR-26a-5p调控PTEN/PI3K/Akt信号通路对高糖诱导视网膜Müller细胞活化及凋亡的影响
- Author:
Derong TANG
1
;
Yuwen YANG
;
Rui SHI
;
Dandan LIU
Author Information
- Keywords: retinal Müller cell; microRNA-26a-5p(miR-26a-5p); PTEN/PI3K/Akt; inflammation; diabetic retinopathy
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2024;45(5):705-711
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the effects of microRNA-26a-5p(miR-26a-5p)on high glucose-induced retina Müller activation and apoptosis by regulating PTEN/PI3K/Akt signaling pathway,and the potential mechanism of diabetic retinal neurodegeneration.Methods Various concentrations of high glucose were added into rMC-1 culture.CCK-8 and flow cytometry was used to examine cell proliferation and apoptosis respectively.The regulatory effects of miR-26a-5p on the expressions of PTEN,PI3K and Akt were observed by real-time PCR;the expression levels of IL-1β and IL-6 in Müller cells were examined by ELISA.The data were processed by Graphpad 8.0 software.Results Müller cells grew actively in high-glucose stimulation culture.Compared with the control group,the activity of Müller cells stimulated by 50 mmol/L glucose increased gradually at 12 h and 24 h,but decreased at 48 h after stimulation,when Müller cells apoptosis increased.The difference between the groups was statistically significant(P＜0.05).The expression of miRNA-26a-5p decreased,that of PTEN increased,and those of PI3K and Akt decreased.Meanwhile,IL-1β and IL-6 levels were significantly increased in Müller cells.miR-26a-5p over-expression alleviated injuries to high glucose stimulated retinal Müller cells by inhibiting PTEN,which upregulated the expression of PI3K/Akt and downregulation of IL-1β and IL-6(P＜0.01).Conclusion Upregulating miR-26a-5p protects Müller cells against apoptosis,probably through regulation of PTEN/PI3K/Akt and affecting the production of inflammatory factors.
