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Notch activates cell cycle reentry and progression in quiescent cardiomyocytes

Víctor M Campa1, Raquel Gutiérrez-Lanza, Fabio Cerignoli

  • 1Burnham Institute for Medical Research, La Jolla, CA 92037, USA.

The Journal of Cell Biology
|October 8, 2008
PubMed

Insights

Notch signaling reactivates cell division in immature heart cells. While it promotes cell cycle entry, mature cells experience arrest, revealing Notch

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Cell Cycle Regulation

Background:

  • The limited regenerative capacity of adult cardiomyocytes hinders heart repair after injury.
  • Understanding factors that control cardiomyocyte proliferation is crucial for regenerative medicine.

Purpose of the Study:

  • To investigate the role of Notch signaling in cardiomyocyte cell cycle re-entry.
  • To elucidate the mechanisms by which Notch signaling influences cardiomyocyte proliferation.

Main Methods:

  • Utilized embryonic stem cell-derived and neonatal ventricular cardiomyocytes.
  • Investigated cell cycle entry and progression.
  • Analyzed gene expression and protein localization, including cyclin D1 and RBP-Jkappa.

Main Results:

  • Notch signaling reactivation induced cell cycle entry in immature cardiomyocytes.
  • Proliferative response diminished with cardiomyocyte maturation, leading to cell cycle arrest.
  • Notch signaling promoted RBP-Jkappa-dependent cyclin D1 expression and nuclear localization.

Conclusions:

  • Notch signaling can stimulate cardiomyocyte proliferation, particularly in immature cells.
  • Maturation-dependent cell cycle arrest is observed with late Notch activation.
  • Notch signaling's effect on cyclin D1 nuclear localization is a novel mechanism with implications for cardiogenesis and tumorigenesis.

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