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. 2023 Sep 26;4(10):101209. doi: 10.1016/j.xcrm.2023.101209

Figure 6.

Figure 6

tRF-3001a-GSK3B signaling axis regulates retinal neurovascular dysfunction in vitro and in vivo

(A and B) Müller cells were transfected with negative control (NC) mimics (Ctrl), tRF-3001a mimics, NC siRNA, GSK3B siRNA, tRF-3001a plus GSK3B overexpression vector, or tRF-3001a plus null vector for 24 h. Cell viability was examined by CCK-8 assays (A, n = 4). Cell proliferation was examined by EdU staining. EdU, green; DAPI, blue. Scale bar, 20 μm (B, n = 4).

(C–G) STZ-induced diabetic mice received intravitreal injections of NC agomir, tRF-3001a agomir, NC shRNA, GSK3B shRNA, tRF-3001a plus GSK3B overexpression vector, or tRF-3001a plus null vector for 2 months. Retinal reactive gliosis (C; scale bar, 50 μm), RGC degeneration (D; scale bar, 50 μm), retinal vasopermeability (E and F; scale bar, 500 μm), and retinal acellular capillaries (G) were detected to evaluate the role of tRF-3001a-GSK3B signaling axis in retinal neurovascular dysfunction in vivo (n = 5). ∗p < 0.05 versus Ctrl group, #p < 0.05 between the marked groups; one-way ANOVA followed by post hoc Bonferroni test. See also Figures S10, S11, and S12.