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  • microRNA-383 mediates high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells by repressing peroxiredoxin 3.

microRNA-383 mediates high glucose-induced oxidative stress and apoptosis in retinal pigment epithelial cells by repressing peroxiredoxin 3.

American journal of translational research (2017-06-01)
Yanyun Jiang, Yanzhi Sang, Qinghua Qiu
ABSTRACT

Hyperglycemia-mediated damage to retinal pigment epithelial (RPE) cells plays a central role in the pathogenesis of diabetic retinopathy. Dysregulation of microRNA (miR)-383 modulates pancreatic beta cell survival in diabetes; however, its role in diabetic retinopathy remains unclear. In this study, we examined the expression of miR-383 in ARPE-19 human RPE cell lines after high glucose treatment and investigated its functions in high glucose-induced reactive oxygen species (ROS) generation and apoptotic responses. The downstream target gene that mediated the action of miR-383 was functionally characterized. It was found that high glucose induced a 2.4-fold increase in miR-383 abundance, compared to ARPE-19 cells treated with normal glucose. Overexpression of miR-383 inhibited cell viability and promoted apoptosis and ROS formation in ARPE-19 cells, which was coupled with deregulation of Bcl-2 and Bax. Peroxiredoxin 3 (PRDX3) expression was repressed by miR-383 in ARPE-19 cells. Restoration of PRDX3 counteracted miR-383-induced ROS generation and apoptosis, while silencing of PRDX3 phenocopied the detrimental effects of miR-383 on ARPE-19 cells. Delivery of anti-miR-383 inhibitors led to an increase of PRDX3 expression and prevented high glucose-elicited ROS formation and apoptosis in ARPE-19 cells. Overall, miR-383 upregulation accounts for high glucose-induced oxidative stress and apoptosis in RPE cells by repressing PRDX3 expression. Targeting miR-383 may have therapeutic potential in the treatment of diabetic retinopathy.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
DL-Cysteine, technical grade
Sigma-Aldrich
Anti-PRDX3 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-PRDX6 (AB1) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Amyloid Protein Non-Aβ Component, ≥80% (HPLC)