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. 2021 Mar 5;6(9):2999–3012. doi: 10.1016/j.bioactmat.2021.01.036

Fig. 4.

Fig. 4

Assessment of angiogenesis post-MI of ICR mice. (A)Immunostaining of treatment and MI-only groups at day 28 post-MI with neovesselmarker IB4 (red) and counterstained with DAPI for nuclei (blue) in ischemic heart injury border zone and infarct zone, respectively.Scale bar = 50 μm. (B) Immunostaining of treatment and MI-only groups at day 28 post-MI with smooth muscle marker (α-SMA) (red) and counterstained with DAPI for nuclei (blue) in ischemic heart injury border zone andinfarct zone, respectively. Scale bar = 50 μm. (C–F) Quantitative analysis of IB4-and α-SMA-positive cells/mm2; values are means ± SD (control group, n = 5; MI-only group, n = 6; suspension groups, n = 7; cell sheetgroup, n = 7). *Cell sheet group (blue) > cell suspension group (purple) with IB4-positive neovessels in border zone (P < 0.05); *cell sheet group (blue) > cell suspension group (purple) with IB4-positive neovessels in infarctzone (P < 0.05); NScell sheet group (blue) > cell suspension group (purple) with α-SMA-positive arterioles in infarct zone (P > 0.05); one-way ANOVA with Tukey comparison test (C, D, F); **cell sheet group (blue) > cellsuspension group (purple) with α-SMA-positive arterioles in border zone (P < 0.01); Kruskal–Wallis H test with Bonferroni correction (E); . MI, myocardial infarction; Sus, suspension; IB4, isolectin B4; DAPI, 4′,6-diamidino-2-phenylindole; α-SMA, α-smooth muscle actin; SD, standard deviation; ANOVA, analysis of variance. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)