K. Reiss et al., MYOCARDIAL-INFARCTION IS COUPLED WITH THE ACTIVATION OF CYCLINS AND CYCLIN-DEPENDENT KINASES IN MYOCYTES, Experimental cell research, 225(1), 1996, pp. 44-54
To determine whether the molecular components implicated in the regula
tion of the cell cycle are activated in myocytes after infarction, the
expression of cyclins E, A, and B and the levels of their associated
kinase activity were measured at 1 and 7 days following surgery. The q
uantity of cdk2 and cdc2 and the level of their kinase activity were a
lso determined. Myocardial infarction was characterized by an increase
in cyclins E, A, and B and cdc2 proteins in the surviving myocytes at
1 and 7 days. Cyclin E, A, and B and cdk2 and cdc2 kinase activity al
so increased. The quantity of cyclins E and A and the level of cyclin
E-associated kinase activity in myocytes after infarction were compara
ble with those measured in neonatal myocytes. Moreover, cdc2 protein a
nd cdc2 kinase activity in myocytes reached levels after infarction wh
ich were similar to those in neonatal myocytes. Thus, myocytes react t
o myocardial infarction by activating cyclins and cyclin-dependent kin
ases which may he coupled with the regeneration of muscle mass and rec
overy of ventricular function. (C) 1996 Academic Press, Inc.