DIFFERENTIAL EXPRESSION OF ALPHA-ENOLASE AND BETA-ENOLASE GENES DURING RAT-HEART DEVELOPMENT AND HYPERTROPHY

We have analyzed the transition between isoforms of the glycolytic enz yme enolase (2-phospho-D-glycerate hydrolyase; EC 4.2.1.11) in rat hea rt during normal and pathological growth. A striking fall in embryonic alpha-enolase gene expression occurs during cardiac development, most ly controlled at pretranslational steps. In fetal and neonatal hearts, muscle-specific beta-enolase gene expression is a minor contributor t o total enolase. Control mechanisms of beta-enolase gene expression mu st include posttranscriptional steps. Aortic stenosis induces a rapid and drastic decrease in beta-enolase transcript level in cardiomyocyte s, followed by the fall in beta-subunit level. In contrast, alpha-enol ase transcript level is not significantly altered, although the corres ponding subunit level increases in nonmuscle cells. We conclude that, like fetal heart, hypertrophic heart is characterized by a high ratio of alpha- to beta-enolase subunit concentrations. This study indicates that the decrease in beta-enolase gene expression may be linked to be neficial energetic changes in contractile properties occurring during cardiac hypertrophy.