Related Experiment Video
Updated: May 10, 2025

High-Throughput Cardiotoxicity Screening Using Mature Human Induced Pluripotent Stem Cell-Derived Cardiomyocyte Monolayers
Published on: March 24, 2023
Matured hiPSC-derived cardiomyocytes possess dematuration plasticity
Fang Meng1,2,3, Maxwell Kwok2,3,4, Yen Chin Hui2,3
1Department of Biology, New York University, New York, NY, USA.
Insights
Mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) can regain plasticity and dedifferentiate when treated with L-type calcium channel blockers or Src kinase inhibitors, impacting their use in heart repair research.
Area of Science:
- Cardiology
- Stem Cell Biology
- Pharmacology
Background:
- Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are vital for studying heart regeneration.
- L-type calcium channel blockers can induce proliferation in mature hiPSC-CMs, but the mechanism is unknown.
- Cardiomyocyte maturation involves centrosome disassembly, a process potentially reversible in hiPSC-CMs.
Purpose of the Study:
- To investigate the mechanism by which L-type calcium channel blockers induce hiPSC-CM proliferation.
- To explore the plasticity of mature hiPSC-CMs in response to pharmacological compounds.
- To identify factors that can induce centrosome reassembly and cell cycle activity in hiPSC-CMs.
Main Methods:
- Small molecule screening to identify compounds inducing centrosome reassembly in hiPSC-CMs.
- Assessing cell cycle activity in hiPSC-CMs and neonatal rat ventricular myocytes (NRVMs) after compound treatment.
- Differential bulk and single-cell RNA transcriptome analysis to evaluate cellular changes.
Main Results:
- Nitrendipine (L-type calcium channel blocker) and 1-NA-PP1 (Src kinase inhibitor) induced centrosome reassembly in a subpopulation of hiPSC-CMs.
- Centrosome-positive hiPSC-CMs showed increased cell cycle activity compared to centrosome-negative cells.
- Transcriptome analysis revealed that mature hiPSC-CMs, but not NRVMs, undergo dematuration upon treatment with nitrendipine or 1-NA-PP1.
Conclusions:
- Mature hiPSC-CMs exhibit plasticity and can dedifferentiate in response to L-type calcium channel blockers and Src kinase inhibitors.
- This dedifferentiation mechanism differs from that in primary cardiomyocytes (NRVMs).
- The plasticity of hiPSC-CMs has significant implications for experimental systems studying cardiomyocyte maturation and heart regeneration.
Abstract:
Human induced Pluripotent Stem Cell-derived cardiomyocytes (hiPSC-CMs) are increasingly used to identify potential factors capable of inducing endogenous cardiomyocyte proliferation to regenerate the injured heart. L-type calcium channel blockers have previously been identified as a class of factors capable of inducing matured hiPSC-CMs to proliferate. However, the mechanism by which L-type calcium channel blockers promote hiPSC-CM proliferation remains unclear. Here we provide evidence that matured hiPSC-CMs possess plasticity to undergo dematuration in response to certain pharmacological compounds. Consistent with primary cardiomyocyte maturation during perinatal development, we found that centrosome disassembly occurs in hiPSC-CMs during plate-based, temporal, maturation. A small molecule screen identified nitrendipine, an L-type calcium channel blocker, and 1-NA-PP1, a Src kinase inhibitor, as factors capable of inducing centrosome reassembly in a subpopulation of hiPSC-CMs. Furthermore, centrosome-positive hiPSC-CMs were more likely to exhibit cell cycle activity than centrosome-negative hiPSC-CMs. In contrast, neither nitrendipine or 1-NA-PP1 induced centrosome reassembly, or cell cycle activity, in neonatal rat ventricular myocytes (NRVMs). Differential bulk transcriptome analysis indicated that matured hiPSC-CMs, but not NRVMs, treated with nitrendipine or 1-NA-PP1 undergo dematuration. ScRNA transcriptome analysis supported that matured hiPSC-CMs treated with either nitrendipine or 1-NA-PP1 undergo dematuration. Collectively, our results indicate that matured hiPSC-CMs, but not primary NRVMs, possess plasticity to undergo dematuration in response to certain pharmacological compounds such as L-type calcium channel blockers and Src-kinase inhibitors. This study shows that once mature, hiPSC-CMs may not maintain their maturity under experimental conditions which may have implications for experimental systems where the state of hiPSC-CM maturation is relevant.
More Related Videos
08:06Generation of Ventricular-Like HiPSC-Derived Cardiomyocytes and High-Quality Cell Preparations for Calcium Handling Characterization
Published on: January 17, 2020
07:02Analyzing the α-Actinin Network in Human iPSC-Derived Cardiomyocytes Using Single Molecule Localization Microscopy
Published on: November 3, 2020