Journal: Frontiers in Immunology
Article Title: METTL3-mediated m6A modification regulates D-galactose-induced skin fibroblast senescence through miR-208a-5p
doi: 10.3389/fimmu.2025.1577783
Figure Lengend Snippet: miR-208a-5p inhibitor rescues MSFs senescence induced by the silence of METTL3. (A) Cellular senescence was assessed via SA-β-gal staining in MSFs transfected with miR-208a-5p mimic for 48 h or co-treated with D-gal and miR-208a-5p inhibitor for 48 h (n=3). Scale bars: 100μm. **p < 0.01, ***p < 0.001. (B) Western blot analysis of P21 and P53 protein expression levels (n=3). **p < 0.01 vs. NC-mimic; ##p < 0.01 vs. NC-inhibitor + D-gal. (C) Scratch wound healing assay demonstrating miR-208a-5p’s effect on cell migration. Wound closure was quantified 12 h post-scratch (n=3). Scale bars, 100μm. **p < 0.01. (D) SA-β-gal staining showing senescence levels in MSFs co-transfected with METTL3 siRNA and miR-208a-5p inhibitor (n=3). Scale bars: 100μm. **p < 0.01 vs. NC-inhibitor; ##p < 0.01 vs. siMETTL3. (E) Proliferative capacity evaluated by EdU incorporation assay (n=3). Scale bars: 50μm. ***p < 0.001 vs. NC-inhibitor; ###p < 0.001 vs. siMETTL3. NC-mimic, negative control mimic; NC-inhibitor, negative control inhibitor.
Article Snippet: A mimic negative control (NC-mimic) and an inhibitor negative control (NC-inhibitor), both sourced from RiboBio (Guangzhou, China), were utilized as the negative controls (NC).
Techniques: Staining, Transfection, Western Blot, Expressing, Wound Healing Assay, Migration, Negative Control