Figure 6.

Short-term CCL2 inhibition in advanced atherosclerosis triggers detrimental changes in plaque phenotype

(A) Acute pharmacological CCL2 inhibition in ApoE^−/− mice after 6 months of western type diet. The anti-CCL2 or isotype control antibody was injected intravenous (i.v.) 2 weeks before sacrifice every 48 h (n = 7–8 / group).

(B) Quantification of fibrous cap coverage as continuity (percentage of fibrous cap covered plaque surface length relative to complete plaque surface length) at three subsequent BCA locations.

(C) Quantification of ACTA2⁺ area within plaque surface as % of plaque surface area (defined as the top 30 μm stripe of the lesion) at three subsequent BCA locations.

(D) Quantification of absolute ACTA2⁺ area in μm² at three subsequent BCA locations.

(E) Quantification of macrophage area as LGALS3 area in μm² at three subsequent BCA locations.

(F) Quantification of total plaque size as absolute plaque area in μm² at three subsequent BCA locations.

(G) Quantification of cell apoptosis as total amount of TUNEL⁺ cells in plaque at three subsequent BCA locations.

(H) Representative images of BCA sections from ApoE^−/− mice after 6 months of western diet stained for ACTA2 (green), LGALS3 (far red), TUNEL (red), and Hoechst (blue). Scale bars, 50 μm.

(I) Quantification of blood leukocytes, neutrophils, lymphocytes, monocytes, and plasma cholesterol (n = 7–8). (I) Student’s t test was used. (B–G) Repeated measures two-way ANOVA or mixed-effects model, with subsequent Šídák’s multiple comparisons test in (B)–(D), was used. ^∗p < 0.05; ^∗∗p < 0.01 NS, not significant. Bar graphs show mean with SEM.