hsa_circ_0041795 contributes to human retinal pigment epithelial cells (ARPE 19) injury induced by high glucose via sponging miR-646 and activating VEGFC.

Diabetic retinopathy (DR)is a common diabetes complication, resulting in the loss of vision. circRNAshave been reported to serve as ceRNA via targeting corresponding miRNAs and modulating mRNA expression in various diseases. Recently, increasing reports has indicated circRNAs can exert a significant role inDR progression. However, the expression and mechanism of hsa_circ_0041795 in human retinal pigment epithelial cells treated by high glucose remains poorly known. Hence, we aimed to work figure out the effect of hsa_circ_0041795 in high glucose (HG)-induced duanyu37E-19 cell damage and study its molecular mechanisms. In our current research, we found that hsa_circ_0041795 was obviously up-regulated in HG-treated duanyu37E-19 cells. High dose of glucose greatly depressed duanyu37E-19 cell survival and contributed to cell apoptosis. In addition, we observed that loss of hsa_circ_0041795 enhanced cell proliferation and inhibit duanyu37E-19 cell apoptosis, after HG incubation. Furthermore, data of ELISA indicated that hsa_circ_0041795 siRNA significantly restrained inflammatory factors expression, such as TNF-α, IL-1β and IL-6 in duanyu37E-19 cells treated with HG. miR-646 has been recognized in multiple diseases and currently, we predicted that miR-646 acted as a target of hsa_circ_0041795. Moreover, we found that miR-646 inhibitors dramatically reversed the effect of hsa_circ_0041795 siRNA on duanyu37E-19 cells. Additionally, a dual-luciferase reporter assay proved that VEGFC was a direct target of miR-646. Our results demonstrated that hsa_circ_0041795 might exhibit a novel therapeutic potential in the treatment of DR.

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