Establishment and functional studies of a model of cardiomyopathy with cardiomyocyte-specific conditional knockout of Arhgef18
Xiaoqiong Fu, Wenjing Yuan, Jiajin Li, Kun Wan, Mei Ge, Bo Pan, Tiewei Lu
TL;DR
A new mouse model with heart-specific deletion of Arhgef18 shows signs of cardiomyopathy, offering a tool to study heart disease mechanisms.
Contribution
A novel cardiomyocyte-specific Arhgef18 conditional knockout mouse model was established for studying cardiomyopathy.
Findings
Arhgef18 cKO mice showed biventricular enlargement and systolic dysfunction.
Knockout mice exhibited cardiomyocyte cytoskeletal rearrangements and polarity disorders.
Nppa and Nppb mRNA levels were elevated in Arhgef18 cKO mice.
Abstract
The rising incidence of cardiomyopathies poses a significant threat to the physical and mental health of patients. The establishment of an animal model that accurately reflects the clinicopathological characteristics of cardiomyopathy is essential for investigating its pathogenesis. In this study, a cardiomyocyte-specific Arhgef18 conditional knockout (cKO) mouse model was established with Cre/LoxP technology, and the results confirmed that the protein encoded by Arhgef18 (Rho/Rac guanine nucleotide exchange factor 18) was knocked out effectively in the myocardium of Arhgef18flox/flox; Nkx2.5-Cre (Arhgef18fl/fl cKO) mice. Compared to Arhgef18fl/fl mice, Arhgef18fl/fl cKO mice presented with slower body weight growth and no differences in survival curves. Cardiac structure and function revealed that Arhgef18fl/fl cKO mice developed biventricular enlargement, ventricular wall thinning and…
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Taxonomy
TopicsCardiomyopathy and Myosin Studies · Viral Infections and Immunology Research · RNA Research and Splicing