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Fibronectin expression in the normal and hypertrophic rat heart
1Department of Biochemistry, Boston University School of Medicine, Massachusetts 02118.
The Journal of Clinical Investigation
|February 1, 1992
Summary
Fibronectin expression, including mRNA and protein, increases in rat ventricles during cardiac hypertrophy induced by L-triiodothyronine or hypertension. Alternative fibronectin splicing also occurs in these models.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Biochemistry
Background:
- Fibronectin is a key extracellular matrix protein involved in cell adhesion and tissue remodeling.
- Cardiac hypertrophy is a significant risk factor for heart failure and involves complex molecular changes.
- Understanding fibronectin's role in cardiac hypertrophy is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the changes in fibronectin expression and splicing during cardiac hypertrophy induced by L-triiodothyronine and mineralocorticoid/salt-induced hypertension.
- To compare the temporal patterns and extent of fibronectin alterations in response to different hypertrophy stimuli.
Main Methods:
- Northern and Western blotting to quantify fibronectin mRNA and protein levels.
- Ribonuclease protection assays to analyze fibronectin isoforms and alternative splicing.
- Induction of cardiac hypertrophy using L-triiodothyronine and mineralocorticoid/salt treatment in rat models.
Main Results:
- Normal rat hearts show higher fibronectin mRNA and protein in atria compared to ventricles.
- L-triiodothyronine-induced hypertrophy increased ventricular fibronectin mRNA and protein, with distinct temporal patterns.
- Mineralocorticoid/salt-induced hypertension also elevated ventricular fibronectin mRNA and protein, alongside alternative splicing.
- Both models exhibited increased fibronectin isoforms containing EIIIA and EIIIB exons during hypertrophy.
- The temporal dynamics and magnitude of fibronectin changes differed between the two experimental models.
Conclusions:
- Fibronectin expression and alternative splicing are altered during cardiac hypertrophy in response to both hormonal and pressure overload stimuli.
- Ventricular fibronectin levels significantly increase during the progression of cardiac hypertrophy.
- Differential regulation of fibronectin isoforms suggests complex roles in cardiac remodeling under pathological conditions.
