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Updated: Jun 26, 2026

Real-Time Measurements of Calcium and Contractility Parameters in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes
Published on: May 26, 2023
Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation
Honghai Liu1, Niyatie Ammanamanchi1, Jocelyn D Mich-Basso2,3
1Department of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.
Cardiomyocyte proliferation involves dynamic changes in calcium transients (CaTs). Reduced Ca2+ at spindle poles, regulated by CDK1 and SERCA2a, is crucial for proper cell division and heart muscle regeneration.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Molecular Cardiology
Background:
- Cardiomyocyte proliferation is essential for heart muscle growth and repair.
- Calcium transients (CaTs) regulate cardiomyocyte contraction but their role in proliferation is unclear.
Purpose of the Study:
- To investigate how calcium signaling adapts during cardiomyocyte proliferation.
- To elucidate the mechanisms controlling Ca2+ dynamics in dividing cardiomyocytes.
Main Methods:
- Monitoring CaT dynamics and Ca2+ levels at spindle poles during cardiomyocyte M phase.
- Investigating the roles of cyclin-dependent kinase 1 (CDK1) and SERCA2a in Ca2+ regulation.
- Utilizing pharmacological inhibition of SERCA2a to assess mitotic disruption.
Main Results:
- Cardiomyocytes exhibit a specific sequence of CaT amplitude changes during M phase.
- Ca2+ levels decrease at spindle poles during prometaphase and metaphase, mediated by dynein 1-dependent SERCA2a.
- Active CDK1 drives both reduced CaT amplitudes and SERCA2a accumulation; CDK1 inhibition reverses these effects.
- Blocking SERCA2a disrupts mitosis, leading to binucleated cardiomyocytes.
Conclusions:
- Changes in Ca2+ signaling are integral to cardiomyocyte proliferation.
- CDK1-mediated regulation of SERCA2a at spindle poles is critical for successful mitosis.
- Precise control of cytosolic Ca2+ levels is essential for heart muscle cell division and regeneration.
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