Fig 1: Cortical levels of pro-inflammatory protein and mRNA markers were increased in the absence of apoA-I. a IL-1β, c PDGFRβ, and d VCAM-1 protein levels were measured by ELISA in soluble half-brain homogenates; values were normalized to total protein concentration in the homogenates. b Il1b mRNA expression was measured in the cortex by qRT-PCR and normalized to β-actin expression. Points represent individual mice, and bars represent mean values. Circles represent female mice, and squares represent male mice. Omnibus analyses of apoA-I and APP/PS1 genotype effects by two-way ANOVA are displayed as exact p values below graphs. Sidak’s multiple comparisons test results are displayed within graphs as *p < 0.05, ***p < 0.001, and ****p < 0.0001. For ELISA, N = 5–19 mice per genotype were used; for mRNA, N = 7–21 mice per genotype were used. apoA-I, apolipoprotein A-I; HEM, hemizygous apoA-I genotype; KO, knockout apoA-I genotype; WT, wildtype APP/PS1 genotype; APP/PS1, transgenic APP/PS1 genotype; IL-1β, interleukin 1 beta; VCAM-1, vascular cell adhesion molecule 1; PDGFRβ, platelet-derived growth factor receptor beta
Fig 2: BAP31 knockout on HUVEC. (A) The effect of BAP31 knockout on ICAM1 expression in cells and its semi-quantitative analysis (Scale bars: 50μm). (B) The effect of BAP31 knockout on VCAM1 expression in cells and its semi-quantitative analysis (Scale bars: 50μm). (C) The effect of BAP31 knockout on ICAM1 and VCAM1 in animal tissues and its semi-quantitative score (Scale bars: 50μm). Values were represented as mean ± SD, *p < 0.05.
Fig 3: Circ_HUWE1 reduces lipid accumulation and inflammation in VSMCs via the miR-143-3p/IGFBP5 axis. (A, B) Oil Red O and BODIPY cholesterol staining of VSMCs under different transfection conditions. Gene expression level of (C) IL-1β, (D) IL-6, (E) TNF-α, (F) IFN-γ, (G) ICAM-1, and (H) VCAM-1 in VSMCs. Data are shown as the mean ± SD from at least three independent experiments, and statistical analyses were performed using one-way analysis of variance (ANOVA) with Tukey’s post-hoc test. *p < 0.05, **p < 0.01, ***p < 0.001
Fig 4: Circ_HUWE1 reduces inflammation in HFD-fed ApoE−/− mice. Serum levels of inflammatory cytokines and adhesion molecules, including (A) IL-1β, (B) IL-6, (C) TNF-α, (D) IFN-γ, (E) ICAM-1, and (F) VCAM-1 in control, HFD, HFD + adv-NC, and HFD + adv-circ-HUWE1 groups mice. Data are shown as the mean ± SD from 7 mice per group, and statistical analyses were performed using one-way analysis of variance (ANOVA) with Tukey’s post-hoc test. *p < 0.01, **p < 0.01, ***p < 0.001
Fig 5: Circ_HUWE1 alleviates lipid accumulation and inflammation in HFD-fed ApoE−/− mice via the miR-143-3p/IGFBP5 axis. (A) Representative images of Oil Red O staining in aortic sinus sections and lipid deposition within lesion area from control, HFD, HFD + adv-NC, HFD + adv-circ-HUWE1, HFD + adv-circ-HUWE1 + agomir-miR-143 and HFD + adv-circ-HUWE1 + sh-IGFBP5 groups. (B-C) Immunohistochemical staining of CD68 and α-SMA. (D-G) Serum levels of TC, TG, LDL and HDL in control, HFD, HFD + adv-NC, HFD + adv-circ-HUWE1, HFD + adv-circ-HUWE1 + agomir-miR-143 and HFD + adv-circ-HUWE1 + sh-IGFBP5 groups. (H-K) Serum levels of IL-1β, IL-6, ICAM-1, and VCAM-1 in control, HFD, HFD + adv-NC, HFD + adv-circ-HUWE1, HFD + adv-circ-HUWE1 + agomir-miR-143 and HFD + adv-circ-HUWE1 + sh-IGFBP5 groups. Data are shown as the mean ± SD from at least three independent experiments, and statistical analyses were performed using one-way analysis of variance (ANOVA) with Tukey’s post-hoc test. *p < 0.05, **p < 0.01, ***p < 0.001
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