Fig 1: Effects of si-CARM1 on HG-induced ARPE-19 cell injury. ARPE-19 cells were transfected with si-con or si-CARM1 and then treated with HG. The cells treated with NG were used as control. (a) The protein expression of CARM1 was detected by the WB analysis. (b) ELISA was used to analyze the concentrations of IL-6 and TNF-a. Cell proliferation and apoptosis were determined using MTT assay (c), EdU assay (d), and flow cytometry (e). (f) The WB analysis was performed to examine the protein expression of Bax and cleaved-caspase-3. (g, h) Cell oxidative stress was analyzed by detecting MDA level and SOD activity. **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Fig 2: Circ-ADAM9 sponged miR-338-3p to regulate CARM1. The mRNA and protein expression of CARM1 was measured by qRT-PCR (a) and WB analysis (b) in ARPE-19 cells co-transfected with si-circ-ADAM9 and anti-miR-338-3p, respectively. ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.
Fig 3: miR-338-3p targeted CARM1. (a) The binding sites between CARM1 3'UTR and miR-338-3p were shown. The interaction between CARM1 and miR-338-3p was verified by dual-luciferase reporter assay (b) and RIP assay (c). (d, e) The mRNA and protein expression of CARM1 in the serum of DR patients and normal control volunteers was detected by qRT-PCR and WB analysis. (f) The correlation between CARM1 and miR-338-3p was analyzed by Pearson's correlation coefficient analysis. (g) The CARM1 protein expression in ARPE-19 cells under HG and NG conditions was determined by the WB analysis. (h) The miR-338-3p expression was detected by qRT-PCR to evaluate the transfection efficiency of miR-338-3p mimic and inhibitor. (i) The protein expression of CARM1 was detected by the WB analysis in HG-induced ARPE-19 cells transfected with miR-338-3p mimic and inhibitor. **P < 0.01, ***P < 0.001, and ****P < 0.0001.
Fig 4: Effects of CARM1 and miR-338-3p on HG-induced ARPE-19 cell injury. (a) The transfection efficiency of pcDNA CARM1 overexpression vector was assessed by detecting CARM1 protein expression using the WB analysis. (b–j) ARPE-19 cells were transfected with miR-NC, miR-338-3p, miR-338-3p + pcDNA, or miR-338-3p + CARM1 and then treated with HG. The cells treated with NG were used as control. (b) The WB analysis was used to measure the protein expression of CARM1. (c) The concentrations of IL-6 and TNF-α were examined using ELISA. Cell proliferation and apoptosis were measured by MTT assay (d), EdU assay (e), and flow cytometry (f, g). (h) The WB analysis was used to detect the protein expression of Bax and cleaved-caspase-3. (i, j) MDA level and SOD activity were determined to assess cell oxidative stress. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.
Fig 5: Molecular mechanism of circZNF532/miR-1243/CARM1 axis in DR. The flow chart displayed the mechanism by which circZNF532 regulated DR progression through miR-1243/CARM1 axis
Supplier Page from Abcam for Anti-CARM1 antibody