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Figure 1

From: Receptor tyrosine kinase inhibitors negatively impact on pro-reparative characteristics of human cardiac progenitor cells

Figure 1

RTKIs reduce CPC survival in vitro and impact upon cardiac function in vivo. RTKIs impact negatively on human CPC viability following (a) 24-h exposures to 1–100 µM IM, 1.25–100 µM SM or 1–100 µM ST (n = 4) and (b) 7-day exposures to 1–5 µM IM, 0.5–3 µM SM or 1–5 µM ST (n = 4). Application of SM to adult male Wistar rats in vivo caused (c) a reduction of cardiac stroke volume after 9 days (n = 12), with (d) similar impact on ejection fraction (n = 12), followed by recovery of both 7 days after cessation of SM. Left ventricular end-diastolic volume (e) was transiently reduced, but LV end-systolic volume (f) was not altered (n = 12). (g) Echocardiography analysis of LV mass, stroke volume and ejection fraction in recovery and non-recovery groups after 9 days’ SM treatment (n = 6). (h) Representative image of immunostaining: α-sarcomeric actin (red), c-kit (green), DAPI (blue) showing CPC in situ (arrow; scale bar = 50 µm). (i) Immunohistochemical analysis of c-kitpos cell number (per mm2) in control, recovery and non-recovery groups (n = 6). (j) Histochemical analysis of cardiac fibrosis in control, recovery and non-recovery groups (n = 6), with (k) representative images of Sirius red collagen staining (scale bar = 750 µm). All data are mean ± SEM; significance was determined by Student’s t-test for (i), or ANOVA with Holm-Šídák post hoc test to identify differences in all other comparisons (*p < 0.05; **p < 0.01; ***p < 0.001).

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