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. 2018 Nov 5;40(17):1362–1373. doi: 10.1093/eurheartj/ehy696

Figure 6.

Figure 6

Platelets accelerate calcific aortic valve stenosis progression in mice. (A) Scanning electron microscope studies of aortic valves (aorta facing side) of C57BL6 and IGFII mice under high-fat, high-sucrose diet and quantification of area ratio occupied with platelets (n = 10). (B) Mouse protocol. (C) Platelet-induced rise of ΔV2 between weeks 16 and 21 was abrogated by treatment with Ki16425 (n = 40). (D) Spearman correlation between platelets-associated autotaxin activity and peak transaortic gradient (n = 34). (E) Scanning electron microscope studies of mice aortic valves (aorta-facing side) showing aggregates of platelets (arrows) and quantification of area ratio occupied with platelets (n = 12). (F) Immunofluorescence analyses show that BMP2 level was elevated in leaflets of mice receiving platelets, but not in mice receiving Ki16425 (n = 27). (G) Leaflets mineralization was quantified by using Osteosense 680 and showed that platelet-induced mineral deposits on aortic valve leaflets was inhibited by Ki16425 (n = 24). Scale bars: (A) 10 µM, inset 1 µM (D) 20 µM (E and F) 200 µM. Ki16425: 5 mg/kg/day (DMSO: 10 µL/mL). Values are presented as mean ± standard deviation. ATX, autotaxin; BMP2, bone morphogenetic protein 2; DAPI, 4′,6-diamidino-2-phénylindole; HFHS, high fat high sucrose; IGFII, LDLR−/− apoB100/100 IGFII transgenic mice; RFU, relative fluorescence unit; ΔV2, delta peak transaortic velocity.