A pilot study on the relationship between miR-181a and RGCs in retinal ischemia-reperfusion injury model
10.3760/cma.j.issn.2095-0160.2015.11.006
- VernacularTitle:微小RNA-181a与视网膜节细胞在视网膜缺血-再灌注中的关系及其作用机制探讨
- Author:
Jinnan, LIU
;
Yu, HE
;
Junjun, ZHANG
;
Wei, FAN
- Publication Type:Journal Article
- Keywords:
Retinal ischemia-reperfusion;
Retinal ganglion cells;
Tumor necrosis factor-α;
microRNA-181a
- From:
Chinese Journal of Experimental Ophthalmology
2015;33(11):985-990
- CountryChina
- Language:Chinese
-
Abstract:
Background Retinal ischemia-reperfusion (RIR) injury is a common pathologic change.Its mechanism has not been identified.Objective This study was to investigate the relationship of microRNA-181a (miR-181a) ,tumor necrosis factor-α (TNF-α) and retinal ganglial cells (RGCs) in RIR injury.Methods RIR models were induced in 68 rats,then the rats were randomly divided into control group and RIR groups,including 0hour group,24-hour group and 72-hour group by random number table.Predicted target gene TNF-α was chosen,according to M iRanda,Targetscan and miRBase databases.Immunofluorescent labeling, Western blot and quantitative real-time PCR were used to identify the expression levels of miR-181a,TNF-α and RGCs.Immunofluorescent labeling of RGCs in retinal flat mounts was analyzed for RGCs counts.Results Compared with the control group, RGCs densitiy was obviously decreased in 24-hour and 72-hour RIR groups (P＜0.001).The expression level of mir-181a significantly decreased with reperfusion time in the RIR groups (P＜0.05).Futhermore, the expression level of miR181a was positively correlated with RGCs numbers (r=0.995 ,P=0.005).TNF-α and miR-181a were mainly located in inner layers of retina.As opposed to the changes in RGCs numbers and miR-181a expression,TNF-α in 24-hour group was obviously higher than that of the 0-hour group, though there was no statistical significance in overall correlation analysis.Conclusions In RIR,miR-181a may be involved in regulating RGCs apoptosis.TNF-α may be a target gene of miR-181 a.Interventions within 24 hours after reperfusion might be critical.Further study of miR181 a may help to explore new molecular targets for neuroprotection treatment.
