Relationship of MMP-14 and TIMP-3 Expression with Macrophage Activation and Human Atherosclerotic Plaque Vulnerability

Figure 3

(a)–(j) Representative images of immunohistochemical labelling of unstable ((a)–(e)) and stable ((f)–(j)) human carotid artery atherosclerotic plaques, for macrophages (CD68, panels (a) and (f)), and colocalisation of nuclear-localised NFκB with MMP-14 ((b)–(d)), and CD206 with TIMP-3 ((h)–(j)), with nuclei counterstained with DAPI (blue). Box in panels (a) and (f) represents higher magnification in panels (b)–(e) and (g)–(j), respectively. Scale bar in (a) represents 250 μm and is applicable to panels (a) and (f), whereas scale bar in (b) represents 100 μm and is applicable to panels (b)–(e) and (g)–(j). Arrows in panels (b)–(d) indicate MMP-14 +ve FCMs with nuclear NFκB. Panels (e) and (j) represent negative controls where the primary antibodies were replaced with the relevant species IgG. (k) The percentage of MMP-14 positive FCMs that also stained for nuclear-localised NFκB was significantly greater () compared to only cytoplasmic NFκB or no staining. (l) The percentage of TIMP-3 positive FCMs that stained also for CD206 was significantly greater () compared to those stained for TIMP-3 or CD206 alone.