• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

Cyclin A2 mediates cardiomyocyte mitosis in the postmitotic myocardium.

Cell cycle withdrawal limits proliferation of adult mammalian cardiomyocytes. Therefore, the concept of stimulating myocyte mitotic divisions has dramatic implications for cardiomyocyte regeneration and hence, cardiovascular disease. Previous reports describing manipulation of cell cycle proteins have not shown induction of cardiomyocyte mitosis after birth. We now report that cyclin A2, normally silenced in the postnatal heart, induces cardiac enlargement because of cardiomyocyte hyperplasia when constitutively expressed from embryonic day 8 into adulthood. Cardiomyocyte hyperplasia during adulthood was coupled with an increase in cardiomyocyte mitosis, noted in transgenic hearts at all time points examined, particularly during postnatal development. Several stages of mitosis were observed within cardiomyocytes and correlated with the nuclear localization of cyclin A2. Magnetic resonance analysis confirmed cardiac enlargement. These results reveal a previously unrecognized critical role for cyclin A2 in mediating cardiomyocyte mitosis, a role that may significantly impact upon clinical treatment of damaged myocardium.

Pubmed ID: 15159393

Authors

  • Chaudhry HW
  • Dashoush NH
  • Tang H
  • Zhang L
  • Wang X
  • Wu EX
  • Wolgemuth DJ

Journal

The Journal of biological chemistry

Publication Data

August 20, 2004

Associated Grants

None

Mesh Terms

  • Animals
  • Cyclin A
  • Gene Expression Regulation
  • Heart Diseases
  • Hyperplasia
  • Mice
  • Mice, Transgenic
  • Mitosis
  • Myocardium
  • Myocytes, Cardiac