MiRNA-138-5p protects the early diabetic retinopathy by regulating NOVA1.

Abstract:

OBJECTIVE:To elucidate the function of miRNA-138-5p in the early diabetic retinopathy (DR) and the potential mechanism. MATERIALS AND METHODS:DR model in rats was first established by streptozotocin (STZ) injection. MiRNA-138-5p expression in rat retinal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Besides, its expression in retinal capillary endothelial cells (EC) and pericytes (RP) was also detected. Cell counting kit-8 (CCK-8) assay was performed to evaluate proliferative potentials of EC and RP cells. The target gene of miRNA-138-5p was predicted by bioinformatics and further confirmed by dual-luciferase reporter gene assay. Rescue experiments were carried out to verify whether the target gene could reverse the regulatory effect of miRNA-138-5p on the proliferation of EC and RP cells. RESULTS:MiRNA-138-5p was lowly expressed in retinal tissues of DR rats, as well as in EC and RP cells. Overexpression of miRNA-138-5p suppressed the proliferative rate of EC and RP cells, and miRNA-138-5p knockdown obtained the opposite trends. NOVA1 was verified to be the target gene of miRNA-138-5p by dual-luciferase reporter gene assay and RIP assay, which was highly expressed in retinal tissues of DR rats, EC, and RP cells. MiRNA-138-5p knockdown markedly upregulated the mRNA and protein levels of NOVA1 in EC and RP cells. Of note, the inhibitory effect of miRNA-138-5p overexpression on proliferative potentials of EC and RP cells was reversed by NOVA1 overexpression. On the contrary, miRNA-138-5p knockdown accelerated their proliferative potentials and was further reversed by NOVA1 knockdown. CONCLUSIONS:MiRNA-138-5p was lowly expressed in retinal tissues of DR rats, as well as in EC and RP cells. MiRNA-138-5p regulates the early DR by promoting cell proliferation via targeting NOVA1.

authors

Bao XY,Cao J

doi

10.26355/eurrev_201909_18984

subject

Has Abstract

pub_date

2019-09-01 00:00:00

pages

7749-7756

issue

18

eissn

1128-3602

issn

2284-0729

journal_volume

23

pub_type

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