Fig. 10
aPC-mediated reversal of hyperglycaemia-induced persistent p66Shc expression and plaque instability depends on DNMT1. a Experimental design. b Representative images of Oil Red O-stained aortic root lesions (left panel) and dot plot summarizing data (right panel). c Dot plots summarizing morphometric analyses of necrotic core area (left panel), fibrous cap thickness (middle panel), and frequency of ruptured shoulders (right panel). d Representative images showing immunofluorescence staining of macrophages within lesions (MOMA-2, green; DAPI nuclear counterstain, blue; left panel) and dot plot summarizing data (right panel). e Representative co-immunofluorescence images for 8-Oxo-dG (red), macrophages (MOMA-2, green), and DAPI nuclear counterstain (blue) within aortic root lesions (left, ×10 magnified images shown in lower panel) and dot plot summarizing data (Icorr, correlation index, right). Cont: normoglycaemic ApoE−/− mice with normal chow diet; DM-NG: ApoE−/− DM mice receiving the SGLT2 inhibitor and PBS from week 16 to week 22; DM-NG-aPC-DNMT1-MO: DM-NG mice with concomitant SGLT2 inhibitor, aPC, and DNMT1-MO treatment; DM-NG-aPC-Cont-MO: DM-NG mice with concomitant SGLT2 inhibitor, aPC, and control morpholino treatment. Data shown as dot plots represent mean ± SEM of 8–10 mice per group; size bars: b, d, e 20 µm; **P < 0.01; b–e one-way ANOVA with Bonferroni-adjusted post hoc comparison of DM-NG and DM-NG-aPC-DNMT1-MO versus DM-NG-aPC-Cont-MO)
