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Pluripotent Stem Cell Derived Cardiac Cells for Myocardial Repair
Published on: February 3, 2017
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Large Cardiac Muscle Patches Engineered From Human Induced-Pluripotent Stem Cell-Derived Cardiac Cells Improve
Ling Gao1, Zachery R Gregorich2, Wuqiang Zhu1
1Department of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham (L.G., W.Z., S.M., Y.O., X.LO., R.K., A.V.B., G.P.W., A.E.P., V.G.F., S.G.L., J.Z.).
Circulation
|December 14, 2017
Summary
Engineered human cardiac muscle patches (hCMPs) show improved cardiac function and reduced infarct size after transplantation in a myocardial infarction model. These patches mature in vitro and promote heart repair without increasing arrhythmias.
Area of Science:
- Regenerative Medicine
- Cardiovascular Biology
- Stem Cell Therapy
Background:
- Development of clinically relevant sized human cardiac muscle patches (hCMPs) using human induced-pluripotent stem cells.
- hCMPs composed of cardiomyocytes, smooth muscle cells, and endothelial cells within a fibrin scaffold.
Purpose of the Study:
- To assess the maturation and therapeutic potential of hCMPs in a preclinical model of myocardial infarction (MI).
- To evaluate the impact of hCMP transplantation on cardiac function, infarct size, and arrhythmogenicity.
Main Methods:
- Fabrication of hCMPs and in vitro maturation via dynamic culture.
- In vivo transplantation of hCMPs into porcine hearts with induced MI.
- Assessment of cardiac function (MRI), infarct size, and engraftment (qPCR).
Main Results:
- hCMPs demonstrated in vitro maturation with improved electromechanical coupling and force generation.
- Transplantation led to significant improvements in left ventricular function and reduced infarct size.
- Engraftment rate was 10.9% at 4 weeks; exosomes showed cytoprotective effects.
Conclusions:
- Clinically relevant sized hCMPs can be fabricated and matured in vitro.
- hCMP transplantation significantly improves cardiac function and reduces infarct size post-MI.
- hCMPs are not associated with increased arrhythmogenicity and may promote repair via exosomes.
