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Tropoelastin Improves Post-Infarct Cardiac Function
Robert D Hume1,2, Shaan Kanagalingam1, Tejas Deshmukh1,3,2
1Centre for Heart Research, Westmead Institute for Medical Research, NSW, Australia (R.D.H., S.K., T.D., S.C., F.N.R., J.L., Z.E.C., E.K., J.J.H.C.).
Circulation Research
|December 1, 2022
Summary
Introducing tropoelastin after myocardial infarction (MI) significantly improved heart function and reduced scar size in rats. This suggests tropoelastin therapy could be a promising treatment for heart repair in humans.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Biomaterials Science
Background:
- Myocardial infarction (MI) leads to scar formation, impairing heart function.
- The extracellular matrix protein elastin, known for its elasticity, may offer superior scar properties compared to collagen.
- This study investigated tropoelastin, the soluble elastin subunit, to enhance cardiac scar mechanics post-MI.
Purpose of the Study:
- To assess the therapeutic potential of tropoelastin in improving cardiac repair after myocardial infarction.
- To investigate the effects of tropoelastin on scar mechanics, cardiac function, and gene expression in a rodent MI model.
- To explore the translational relevance of tropoelastin in human cardiac disease.
Main Methods:
- Developed an ultrasound-guided intramyocardial injection technique for tropoelastin delivery in a rat MI model.
- Administered tropoelastin or PBS vehicle control to infarcted rat hearts.
- Utilized echocardiography, histological assessments, and RNA sequencing (RNAseq) to evaluate cardiac function, scar characteristics, and gene expression.
- Analyzed human cardiac samples for tropoelastin and ELN gene expression.
Main Results:
- Tropoelastin significantly improved left ventricular ejection fraction and reduced dyssynchrony compared to controls.
- Histological analysis revealed reduced scar size and increased scar elastin content in tropoelastin-treated rats.
- RNAseq showed tropoelastin upregulated genes for elastic fiber formation and downregulated immune response genes post-MI.
- Human cardiac samples demonstrated increased tropoelastin in fibrotic areas and upregulated ELN gene expression.
Conclusions:
- Direct intramyocardial injection of tropoelastin significantly improves cardiac function and reduces scar size in a rodent model of MI.
- Tropoelastin promotes elastic fiber formation and modulates immune response in the infarcted heart.
- Findings suggest tropoelastin is a promising therapeutic agent for cardiac repair, with potential for clinical translation in treating heart disease.
