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Cardiac remodeling in Gαq and Gα11 knockout mice
Kathrina Wiesen1, Elisabeth Kaiser2, Laura Schröder2
1Institute of Veterinary Physiology, Vetsuisse Faculty and the Zürich Center for Integrative Human Physiology, University of Zürich, 8057 Zürich, Switzerland; Institute for Molecular Cell Biology and Research Centre for Molecular Imaging and Screening, Saarland University, 66421 Homburg/Saar, Germany.
Gαq/Gα11 signaling is crucial for maintaining cardiac extracellular matrix properties. Disrupting these pathways impacts gene activity and may influence cardiac hypertrophy development.
Area of Science:
- Cardiovascular Biology
- Molecular Signaling
- Cardiac Physiology
Background:
- Gαq and Gα11 protein signaling are implicated in cardiac hypertrophy.
- Their precise roles in myocardial function require further elucidation.
Purpose of the Study:
- To investigate the specific contributions of Gαq and Gα11 signaling to cardiac remodeling and function.
- To analyze the impact of altered Gαq/Gα11 expression on myocardial properties and extracellular matrix.
Main Methods:
- Utilized genetically modified mouse models: Gα11-knockout, cardiac-specific inducible Gαq-knockout, and double knockout (dKO).
- Employed echocardiography, telemetric ECG, histological analysis (collagen staining), and transcriptome analysis.
Main Results:
- dKO mice exhibited increased ejection fraction and decreased heart rate, maintaining cardiac output, attributed to Gα11 absence and reduced afterload.
- Histology revealed diminished collagen in aging dKO hearts.
- Transcriptome analysis showed altered gene activity related to extracellular matrix regulation, including Cyr61.
Conclusions:
- Gαq/Gα11 signaling pathways are vital for maintaining cardiac gene activity patterns.
- These pathways are important for modulating the extracellular matrix in the heart.
- This modulation may contribute mechanistically to pressure-overload induced cardiac hypertrophy.
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