Involvement of micro RNA-181a and Bim in a rat model of retinal ischemia-reperfusion injury

• Published in: 国际眼科杂志：英文版 Vol. 9; no. 1; pp. 33 - 40
• Main Author: Yu He Jin-Nan Liu Jun-Jun Zhang Wei Fan
• Format: Journal Article
• Language: English
• Published: 2016
• ISSN: 2222-3959; 2227-4898

AIM：To investigate the changes in the expression of micro RNA-181a（mi R-181a）and Bim in a rat model of retinal ischemia-reperfusion（RIR）,to explore their target relationship in RIR and their involvement in regulating apoptosis of retinal ganglion cells（RGCs）.·M ETHODS：Target gene prediction for mi R-181a was performed with the aid of bioinformatics and Bim was identified as a potential target gene of mi R-181a.A rat model of RIR was created by increasing the intraocular pressure.RGCs in the flatmounted retinas were labeled with Brn3,a marker for alive RGCs,by immunofluorescent staining.The changes in the number of RGCs after RIR were recorded.Quantitative reverse transcription-polymerase chain reaction（q RT-PCR）was used to determine the expression level of mi R-181a in the retina.Bim/Brn3 double immunofluorescence was used to detect the localization of Bim.The expression of Bim in the retina was determined with the aids of Western blot and q RT-PCR.·R ESULTS：Compared with the negative control group,the density of RGCs was significantly lower in the ischemia/reperfusion（I/R）-24h and I/R-72h groups（〈0.001）.The expression level of mi R-181a started to decrease at 0h after RIR,and further decreased at 24h and 72h compared with the negative control group（〈0.001）.Bim was significantly upregulated at 12h after RIR（〈0.05）and reached peak at 24,72h compared with the negative control group（〈0.01）.Pearson correlation analysis showed that the expression level of Bim was negatively correlated with the expression level of mi R-181a and the density of RGCs.·CONCLUSION：Bim may be a potential target gene of mi R-181a.Both mi R-181a and Bim are involved in RGCs death in RIR.RIR may promote RGCs apoptosis in the retina downregulation of mi R-181a and its inhibition on Bim expression.