Fig. 5. RvD1 limits necrosis and p16^INK4A positive cells and increases collagen in progressing plaques from sublethally irradiated Ldlr^−/− mice.

(A, B) Representative H&E image and quantification of percent necrosis of lesion area in mock, Vehicle (IR) or RvD1 (IR+RvD1) treated sublethally irradiated-Ldlr^−/− mice. Magnification is 20X, and the scale bar is 50μm. (C, D) Representative picrosirius red images and quantification of percent picrosirius red area in mock, IR or IR+RvD1 mice. The magnification is 10X and the scale bar is 100μm. (E, F) Representative p16^INK4A immunofluorescence images and quantification of p16^INK4A+ lesion cells are shown. White stars represent p16^INK4A+ cells and p16^INK4A is shown in magenta, whereas nuclei are stained in blue with DAPI. Magnification is 40X and the scale bar is 50μm. (G, H) Immunohistochemistry of p16^INK4A in human coronary atherosclerotic lesions from non-cancer patients (NC), patients diagnosed with cancer but not treated with radiation (NR) and those with cancer and radiation treatment (R). (G) Whole artery cross-sections are shown on the top, and a higher magnification (within the boxed region) is shown on the bottom. The scale bars are 1mm and 200μm, respectively and display p16^INK4A+ cells in brown. (H) Quantification of the percent of p16^INK4A cells per total lesional cells is shown from five different arterial beds from 3 separate patients per group. (B, D, F) Each symbol represents an individual mouse. All results are expressed as mean ± S.E.M., analyzed by One-way ANOVA with Tukey’s post-hoc test. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, ns – non-significant.