beta-Adrenergic stimulation controls the expression of a thioesterase specific for very-long-chain fatty acids in perfused hearts.

NEUMAN ISABEL; MALOBERTI PAULA; LISDERO CONSTANZA; COLONNA CECILIA; PERALTA JORGE; PODEROSO JUAN JOSE; PODESTÁ ERNESTO J.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

ACADEMIC PRESS INC ELSEVIER SCIENCE

Lugar: San Diego; Año: 2002 vol. 299 p. 135 - 141

0006-291X

Arachidonic acid is not freely stored in the cells. A number of different pathways for the mobilization of this compound have been proposed, including a novel mechanism that involves the release of arachidonic acid from arachidonoyl-CoA by a thioesterase with substrate specificity for very-long-chain fatty acids. In rat heart, the acyl-CoA thioesterase activity can be regulated by a mechanism that involves beta-adrenoceptors. In this paper we demonstrate that beta-adrenergic agonists also regulate the acyl-CoA thioesterase mRNA levels. Isoproterenol (10(-7)M)-a concentration known to exert physiological responses-increases in a time-dependent manner the acyl-CoA thioesterase mRNA levels, an effect blocked by a specific beta-adrenoceptor antagonist. In addition, our results show that cAMP is involved in this process. The acyl-CoA thioesterase mRNA levels are also increased by fasting, but not by di(2-ethylhexyl)phthalate, a peroxisome proliferator. These results may suggest the existence of a beta-adrenoceptor-activated regulatory pathway for arachidonic acid release in cardiac tissue.