Fig. 5: Ahr deletion impairs neonatal heart regeneration.
In one set of experiments, Ahr −/− and wild-type mice underwent apical resection (AR) surgery at P1. In another set of experiments, Ahr −/− and wild-type mice were intraperitoneally injected with Kyn at 100 mg/kg every other day from P1 to P28 and underwent AR surgery at P6. a–c Mice were collected at P28 for the cardiac fibrosis formation and function analysis. a Representative images and quantitation of fibrosis area by Masson staining (n = 6/group. *P = 0.0001, # P = 0.0422). b, c Echocardiography analysis of LVEF (b, *P = 0.0140, # P = 0.0258) and LVFS (c, *P = 0.0253, # P = 0.0283) (n = 8/group). d–g, on day 4 after the surgery, the expressions of AHR, KI67, CD31, and VEGFA were evaluated by immunofluorescence staining. d Representative images of immunostaining of AHR in the cytoplasm (yellow arrows) and nuclear (white arrows) for six mice of each group and five images of each mouse were collected. e CM proliferation was analyzed by co-staining of KI67 with TNT (n = 6/group. *P = 0.0475, # P = 0.0353). f Immunostaining of CD31 showing angiogenesis (n = 6/group. *P = 0.0189, # P = 0.0265). g Co-staining of VEGFA and α-SMC in coronary endothelium (n = 6/group. *P = 0.0033, # P = 0.0659). Bar = 500 µm for (a). Bar = 20 µm for (d–g). Data are mean ± SD. *P < 0.05 by one-way ANOVA followed by Tukey’s multiple comparisons.
