International Journal of Molecular Zoology 2024, Vol.14, No.1, 18-21 http://animalscipublisher.com/index.php/ijmz 20 Figure 3 Heart contraction impairs in the ACTA2 G148R variant Figure 4 shows the decrease of cell proliferation in the heart of zebrafish with ACTA2 G148R variant on the the fourth day after fertilization. Compared with the wild-type (WT), zebrafish with ACTA2 p.G148R and ACTA2 p.R179H showed a decrease in the number of proliferative cells (indicated by the white arrow) in the myocardial wall region by using immunostaining techniques with proliferative cell labeling PCNA (red) and DAPI co staining (blue). In the endothelial region, all pathogenic variants of endothelial cells (indicated by yellow arrows) also showed decreased proliferation. The data from part B and C show that the ACTA2 G148R and R179H variants significantly reduced the proliferation of myocardial and endothelial cells. These results may suggest that these specific mutations in the ACTA2gene have adverse effects on heart development and repair ability. Figure 4 Proliferating cells were reduced in the ACTA2 G148R variant 2 Analysis of Research Findings This study demonstrates the effects of ACTA2 G148R and R179H variants on left ventricular non compression and abnormal cardiac morphology, particularly in terms of increased heart rate and decreased cardiac contractility, as well as decreased cell proliferation ability within the heart. The study emphasizes the previously unknown importance of the ACTA2 gene in multiple aspects of cardiovascular development, revealing the molecular
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