MYOCARDIAL-INFARCTION IS COUPLED WITH THE ACTIVATION OF CYCLINS AND CYCLIN-DEPENDENT KINASES IN MYOCYTES

Citation
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
Citations number
51
Categorie Soggetti
Oncology,"Cell Biology
Journal title
ISSN journal
00144827
Volume
225
Issue
1
Year of publication
1996
Pages
44 - 54
Database
ISI
SICI code
0014-4827(1996)225:1<44:MICWTA>2.0.ZU;2-8
Abstract
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.