Targeted deletion of miR-182 leads to photoreceptor dysfunction in mice

Abstract

Purpose : MiR-182 is the most abundantly retinal miRNA in mammals. Although the deletion of miR-182 reveals none apparently structural abnormalities in the retina, the role of miR-182 in the retinal function remains unclear yet. In this study, we aimed to determine whether ablation of miR-182 alters photoreceptor function based on the miR-182 knock out (KO) mice we generated previously.

Methods : The color fundus camera and high resolution spectral-domain optical coherence tomography (SD-OCT) were utilized to screen the morphological and structural changes for the fundus and retinal layers of miR-182 KO mice. Ganzfeld electroretinagram (ERG) was carried out to examine the retinal function. Quantitatively compensational expression of other two members of miR-183 clusters (miR-96 and miR-183) within retina of the miR-182 KO mice was determined using qRT-PCR. Potential target genes of miR-182 were computated and verified though the bioinformatics and RNAseq. Two-tailed student's t-test was used for statistical analysis.

Results : We did not observe retinal structural change in color fundus photograph (FP) and SD-OCT imaging as well as compensational expression of miR-96 and miR-183 in the KO mice. Scotopic ERG showed that both a-wave and b-wave amplitude were decreased. In addition, maximal and photopic ERG were abnormal. Furthermore, we found up-regulated different expression genes in the retina of miR-182 mice.

Conclusions : In summary, we for the first time determined the retinal functional defect in the miR-182 KO mice. Our finding suggested that the miR-182 maybe play a critical role in maintaining the functionality of photoreceptors in mice.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.