Differential expression of a and b enolase genes during rat heart
development and hypertrophy.
Keller, Anglica, Jean-Denis Rouzeau, Farah Farhadian, Claudine
Wisnewsky[acute]i, Fran[grave]ioise Marotte, Noael Lamand, Jane-Lyse
Samuel, Ketty Schwartz[acute]i, Monique Lazar, Marguerite Lucas.
Coll[angstrom]age de France, Biochimie Cellulaire, CNRS URA 1115,
11, Place Marcelin Berthelot, 75231 Paris Cedex 05 France.INSERM U
127, H[diaeresis]opital Lariboisi[angstrom]are 75010 Paris France,
[acute]i INSERM U 153, H[diaeresis]opital Piti[umlaut]a
-Salp[acute]etri[angstrom]are 75013 Paris France
APStracts 2:0253H, 1995.
We have analyzed the transition between isoforms of the glycolytic
enzyme enolase in rat heart, during normal and pathological growth.
During cardiac development a striking fall in embryonic a enolase
gene expression occurs, mostly controlled at pretranslational steps.
In fetal and neonatal hearts, muscle-specific b enolase gene
expression is a minor contributor to total enolase. Control
mechanisms of b enolase gene expression must include post
-transcriptional steps. Aortic stenosis induces a rapid and drastic
decrease in b enolase transcript level in cardiomyocytes, followed by
the fall in b subunit level. In contrast, a enolase transcript level
is not significantly altered, although the corresponding subunit
level increases in nonmuscle cells. We conclude that, like fetal
heart, hypertrophic heart is characterized by a high ratio of a/b
enolase subunit concentrations. This study indicates that the
decrease in b enolase gene expression may be linked to beneficial
energetic changes in contractile properties occuring during cardiac
hypertrophy.
Received 21 February 1995; accepted in final form 1 June 1995.
APS Manuscript Number H157-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.