Fig. 6: MUL1 evaluation in a human model of cardiac hypertrophy and functional insights in an in vivo transgenic mice MUL1 model.

A CM-hiPSC matured for 30 days were treated with NE (10 μM) for 10 days. CM-hiPSC were stained with rhodamine-phalloidin. Nuclei were stained with DAPI. Images were captured using confocal microscopy (upper panel). Scale bar = 50 μm. Cell area was determined (lower panel) (N = 4). B ANP (N = 4), BNP (N = 4), and MUL1 (N = 4) mRNA levels were determined by RT-qPCR. 18S RNA was used to normalize the data. The values correspond to the mean ± SEM. Each independent experiment is displayed as a dot in the graphs. Results were analyzed using a student T-test. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. Cardiac hypertrophic markers were evaluated in a transgenic mouse model overexpressing MUL1 (TG) and their respective wild-type controls (WT). C Expression levels of MUL1 mRNA and the hypertrophic marker ANP were measured in male and female mice at 37 weeks of age (MUL1: N = 7 WT male; N = 8 TG Male, N = 3 WT female, N = 3 TG female; ANP: N = 6 WT male; N = 6 TG Male, N = 3 WT female, N = 3 TG female). D Heart weight-to-tibia length ratio evaluation in male and female WT and TG mice (N = 5 WT male, N = 5 TG male, N = 8 WT female, N = 7 TG female). E Cardiomyocyte cross-sectional area (CSA) analysis in WT and TG male and female 37 weeks mice (N = 6 WT male, N = 8 TG male, N = 4 WT female, N = 4 TG female). Values correspond to the mean ± SEM. Each animal is displayed as a dot in the graphs. The data were analyzed using a Mann-Whitney nonparametric test. *p < 0.05, and ***p < 0.001.