Figure 2.

tRF-3001a regulates Müller cell function following diabetic stress in vitro

(A) Primary Müller cells were transfected with the negative control (NC) mimics, tRF-3001a mimics, NC inhibitors, or tRF-3001a inhibitors or were left untreated (Ctrl) for 24 h. The levels of tRF-3001a were determined by qRT-PCRs (n = 4, ∗p < 0.05 versus Ctrl, one-way ANOVA followed by Bonferroni test).

(B–F) Primary Müller cells were transfected with NC mimics, tRF-3001a mimics, NC inhibitors, or tRF-3001a inhibitors or were left untreated (WT) for 6 h and then exposed to high glucose (25 mM) for 48 h. The group without high-glucose exposure was taken as the control (Ctrl) group. Cell viability was examined by CCK-8 assays (B, n = 4). Cell proliferation ability was examined by EdU staining and quantitated. EdU, green; DAPI, blue. Scale bar, 20 μm (C, n = 4). TUNEL assays were used to detect the apoptosis of Müller cells. TUNEL, green; DAPI, blue. Scale bar, 50 μm (D, n = 4). The dead or dying cells were detected by Calcein-AM/PI staining. Calcein-AM, green; PI, red. Scale bar, 20 μm (E, n = 4). Rhodamine 123 staining was used to detect the change of mitochondrial membrane potentials (ΔΨm) in Müller cells. Rhodamine 123, green; DAPI, blue. Scale bar, 20 μm (F, n = 4). ∗p < 0.05 versus Ctrl; ^#p < 0.05 between the marked groups. The significant difference was evaluated by one-way ANOVA followed by post hoc Bonferroni test. See also Figures S1, S2, and S3.