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Ruxu Sun, Daidi Yang, Chao Jiang, Xue Chen, Qinghuai Liu; LINC00167 regulates RPE differentiation by targeting the miR-203a-3p/SOCS3 axis. Invest. Ophthalmol. Vis. Sci. 2020;61(7):3095.
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Increasing evidence has indicated that long non-coding RNAs (lncRNAs) play significant roles in various diseases, while their roles in age-related macular degeneration (AMD) remain unclear. Dedifferentiation and dysfunction of retinal pigment epithelium (RPE) cells have been shown as contributors to AMD by several studies. We previously found that lncRNA LINC00167 was down-regulated in RPE-choroid samples of AMD patients. In this study, we aimed to find out if LINC00167 participated in RPE dedifferentiation and its underlying mechanism.
The expression of LINC00167 in AMD patients as well as during RPE differentiation were confirmed by microarray. Western blot and immunofluorescence were utilized as measurements of RPE markers. Vascular endothelial growth factor A (VEGFA ) secretion was determined by enzyme linked immunosorbent assay to assess RPE function. Latex beads were used to examine RPE phagocytic ability. Luciferase reporter assay was conducted to prove interaction between LINC00167 and miR-203a-3p. Gene set enrichment analysis was used to identify relationship between LINC00167 and JAK/STAT pathway.
In vitro study indicated that reduced endogenous LINC00167 expression resulted in RPE dedifferentiation, which was typified by attenuated expression of RPE markers, interrupted phagocytic ability and reduced VEGFA secretion in RPE. Mechanistically, LINC00167 functioned as a sponge for miR-203a-3p to restore the expression of SOCS3, which further inhibited the JAK/STAT signaling pathway.
Our study demonstrated that LINC00167 showed a protective role in AMD by maintaining RPE differentiation through LINC00167/miR-203a-3p/SOCS3 axis and might be a potential therapeutic target for AMD.
This is a 2020 ARVO Annual Meeting abstract.
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