Altered Expression of Cell Cycle Proteins and Prolonged Duration of Cardiac Myocyte Hyperplasia in p27 KIP1 Knockout Mice - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Circulation Research Année : 1999

Altered Expression of Cell Cycle Proteins and Prolonged Duration of Cardiac Myocyte Hyperplasia in p27 KIP1 Knockout Mice

Robert Poolman
  • Fonction : Auteur
Jian-Mei Li
  • Fonction : Auteur
Gavin Brooks
  • Fonction : Auteur

Résumé

-The precise role of cell cycle-dependent molecules in controlling the switch from cardiac myocyte hyperplasia to hypertrophy remains to be determined. We report that loss of p27(KIP1) in the mouse results in a significant increase in heart size and in the total number of cardiac myocytes. In comparison to p27(KIP1)+/+ myocytes, the percentage of neonatal p27(KIP1)-/- myocytes in S phase was increased significantly, concomitant with a significant decrease in the percentage of G(0)/G(1) cells. The expressions of proliferating cell nuclear antigen, G(1)/S and G(2)/M phase-acting cyclins, and cyclin-dependent kinases (CDKs) were upregulated significantly in ventricular tissue obtained from early neonatal p27(KIP1)-/- mice, concomitant with a substantial decrease in the expressions of G(1) phase-acting cyclins and CDKs. Furthermore, mRNA expressions of the embryonic genes atrial natriuretic factor and alpha-skeletal actin were detectable at significant levels in neonatal and adult p27(KIP1)-/- mouse hearts but were undetectable in p27(KIP1)+/+ hearts. In addition, loss of p27(KIP1) was not compensated for by the upregulation of other CDK inhibitors. Thus, the loss of p27(KIP1) results in prolonged proliferation of the mouse cardiac myocyte and perturbation of myocyte hypertrophy.

Dates et versions

hal-02561090 , version 1 (03-05-2020)

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Citer

Robert Poolman, Jian-Mei Li, Beatrice Claude Durand, Gavin Brooks. Altered Expression of Cell Cycle Proteins and Prolonged Duration of Cardiac Myocyte Hyperplasia in p27 KIP1 Knockout Mice. Circulation Research, 1999, 85 (2), pp.117-127. ⟨10.1161/01.res.85.2.117⟩. ⟨hal-02561090⟩
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