Abstract
Hypertrophic (HCM) or dilated cardiomyopathy (DCM) can be caused by missense mutations in alpha-tropomyosin (TPM1). In this study, we focus on the TPM1 mutations E62Q (HCM) and E54K (DCM), which were introduced homozygously into separate induced pluripotent stem cell (iPSC) lines using CRISPR/Cas9. iPSC-derived cardiomyocytes were seeded into decellularized myocardial sections to form human engineered heart tissues (EHT) that are suitable for biomechanical evaluation of muscle phenotypes. After two weeks in culture, E62Q EHTs displayed a nearly 3-fold increase in peak isometric twitch force relative to isogenic control with no change in relative slope of length dependent activation.
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