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. 2021 Apr 20;29(8):2554–2570. doi: 10.1016/j.ymthe.2021.04.018

Figure 1.

Figure 1

Improved cardiac function by hAM-MSC-dressing therapy in a rat ICM model

4 weeks after left coronary artery ligation in rats, a hAM-MSC-dressing (fibrin sealant film containing 2 × 106 hAM-MSCs; hMSC-dressing group), a fibrin sealant film only (no cell-dressing group), or nothing (no treatment; ICM group) were placed onto the heart surface. (A) Cardiac function and dimensions assessed by using echocardiography before treatment (day 0 = 4 weeks post-MI) and day 28 post-treatment. LVEF, left ventricular ejection fraction; LVEDV, left ventricular end-diastolic volume; LVDSV, left ventricular end-systolic volume; n = 7−10 in each group. ∗p < 0.05 and ∗∗∗p < 0.001 versus both ICM and no cell-dressing groups. One-way ANOVA with Tukey’s post hoc tests for multiple comparisons. Data presented as mean ± SEM. (B) Echocardiography indexes measured at day 90 post-treatment showing a longer-term effect of hAM-MSC-dressing therapy. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. n = 4−6 in each group. Student’s t test. (C) Macroscopic and immunohistolabeling images of the hearts collected at days 3 and 28 post-hAM-MSC-dressing therapy. Immunolabeling samples were co-stained for cardiac troponin T (cTnT) and 4′,6-diamidino-2-phenylindole (DAPI). Donor hAM-MSCs were labeled with CM-DiI (red) before transplantation. Scale bars, 1 mm or 100 μm for macro- and micro-images. (D) Quantitative cell retention of hAM-MSCs in the rat LV tissue assessed by analyzing genomic DNA (gDNA) levels of the primate-specific ALU gene by qPCR at days 3 and 28 after epicardial placement of hAM-MSC-dressing (including 2 × 106 hAM-MSCs). n = 5 hearts with 3 technical replicates in each time point.