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. 2013 Jun;182(6):2241–2253. doi: 10.1016/j.ajpath.2013.02.011

Figure 1.

Figure 1

Vessel wall thickening, cell number, and vessel diameter are reduced, but apoptosis and proliferation are increased after injury of the femoral artery in Col8−/− mice. A and B: Representative cross-sections of injured femoral arteries from Col8+/+ and Col8−/− mice, respectively, at 21 days after injury. Black circles show the location of the internal elastic lamina. Scale bars: 200 μm. C: Cell number in the media (black bars) and intima (gray bars) and total cell number (sum of black and gray bars) in Col8+/+ (n = 14) and Col8−/− (n = 12) mice at 21 days after injury. ∗P ≤ 0.05, significant difference in medial cell number between genotypes. †P ≤ 0.05, difference in total cell number between genotypes. D: Vessel wall medial and neointimal area at 21 days after wire injury. E: Vessel diameter at 21 days after wire injury. F: Cell proliferation in the media measured at 7 days after injury via Ki-67 immunostaining of sections from Col8+/+ (n = 3) and Col8−/− (n = 4) mice. G: Apoptosis was quantified by measuring the percentage of TUNEL-positive cells in the media at 7 days in Col8+/+ (n = 3) and Col8−/− (n = 3) mice. D–G: Black bars represent the values from Col8+/+ mice, and white bars represent the values from Col8−/− mice. ∗P ≤ 0.05. H and I: Representative cross-sections of injured femoral arteries from Col8+/+ mice (H) and Col8−/− mice (I), respectively, at 7 days after injury, stained for Ki-67. Scale bars: 100 μm.