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Analysis of Cardiomyocyte Development using Immunofluorescence in Embryonic Mouse Heart
Published on: March 26, 2015
Integrin activation and focal complex formation in cardiac hypertrophy
1Cardiology Division of the Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina and the Ralph H. Johnson Department of Veterans Affairs MedicalCenter, Charleston 29425-2221, USA.
The Journal of Biological Chemistry
|August 26, 2000
Summary
Cardiac hypertrophy involves extracellular matrix (ECM) remodeling and cardiocyte growth. This study reveals ECM proteins fibronectin and vitronectin activate signaling pathways like ERK1/2 in pressure-overloaded hearts, impacting cardiac function.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Extracellular Matrix Research
Background:
- Cardiac hypertrophy involves extracellular matrix (ECM) remodeling and cardiocyte growth.
- Integrin-mediated signaling pathways are crucial in cardiac cell responses to mechanical stress.
Purpose of the Study:
- To investigate the role of ECM proteins fibronectin and vitronectin in pressure-overloaded cardiac hypertrophy.
- To elucidate the signaling pathways activated by integrin engagement with ECM proteins in cardiomyocytes.
Main Methods:
- Analysis of ECM protein expression and cytoskeletal association in pressure-overloaded feline myocardium.
- Investigating focal adhesion kinase (FAK), c-Src, and ERK1/2 activation.
- Using synthetic peptides with Arg-Gly-Asp (RGD) motif to stimulate cardiomyocytes cultured in different matrices.
Main Results:
- Increased fibronectin and vitronectin expression and cytoskeletal association in hypertrophied myocardium.
- Pressure overload induced cytoskeletal binding and phosphorylation of FAK and c-Src, and ERK1/2 activation.
- RGD peptide stimulation activated ERK1/2 in cardiomyocytes on laminin or collagen; cytoskeletal assembly of signaling proteins occurred primarily in collagen-embedded cells.
Conclusions:
- Integrin engagement with ECM proteins activates multiple signaling pathways in pressure-overloaded hearts, including focal complex formation and ERK1/2 activation.
- These pathways can be initiated in cardiomyocytes via RGD-stimulated integrin activation, suggesting a role in cardiac remodeling.
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