Preliminary analysis of cell cycle regulation in cardiomyocytes.

抄録

While embryonic cardiomyocytes actively proliferate, this activity is lost shortly after birth in mammals, the mechanisms of which are unknown. At birth, cardiomyocytes are exposed to dramatic changes, including 1) abrupt elevation of oxygen tension by the onset of breathing (PaO₂: 20mmHg to 100mmHg), 2) temporary starvation due to the loss of maternal blood supply, and 3) drastic hemodynamic changes. Here we focused on the effect of 1). The exposure of fetal mouse cardiomyocytes to atmospheric O₂ (20%) inhibited cell proliferation which was evaluated by cell counting and Ki67 expression, suggesting increased O₂ exposure at birth is fundamental for cell cycle exit. To identify the critical genes, microarray was performed with two sample sets, i.e. fetus vs neonate, and fetal cardiomyocytes cultured under 3% vs 20% O₂. We identified 53 genes showing the common expression profile in the two arrays, and are now exploring each phenotype by knock-down experiments.