15deoxy D12,14PGJ2 and PPARgamma levels in term placental tissues from control and diabetic rats. Modulatory effects of the PPARgamma agonist on the nitridergic and lipid placental metabolism

CAPOBIANCO EVANGELINA; JAWERBAUM ALICIA; ROMANINI M CRISTINA; WHITE VERÓNICA; PUSTOVRH CAROLINA; HIGA ROMINA; MARTÍNEZ NORA; MUGNAINI M TERESA; SOÑEZ CARLOS; GONZÁLEZ ELIDA

REPRODUCTION FERTILITY AND DEVELOPMENT

CSIRO PUBLISHING

Lugar: Peth, Australia; Año: 2005 vol. 17 p. 423 - 433

1031-3613

15-Deoxy-Delta(12,14)-prostaglandin J2 (15dPGJ2) is a peroxisome proliferator-activated receptor gamma (PPARgamma) ligand that regulates lipid homeostasis and has anti-inflammatory properties in many cell types. We postulated that 15dPGJ2 may regulate lipid homeostasis and nitric oxide (NO) levels in term placental tissues and that alterations in these pathways may be involved in diabetes-induced placental derangements. In the present study, we observed that, in term placental tissues from streptozotocin-induced diabetic rats, 15dPGJ2 concentrations were decreased (83%) and immunostaining for nitrotyrosine, indicating peroxynitrite-induced damage, was increased. In the presence of 15dPGJ2, concentrations of nitrates/nitrites (an index of NO production) were diminished (40%) in both control and diabetic rats, an effect that seems to be both dependent on and independent of PPARgamma activation. Exogenous 15dPGJ2 did not modify lipid mass, but decreased the incorporation of (14)C-acetate into triacylglycerol (35%), cholesteryl ester (55%) and phospholipid (32%) in placenta from control rats, an effect that appears to be dependent on PPARgamma activation. In contrast, the addition of 15dPGJ2 did not alter de novo lipid synthesis in diabetic rat placenta, which showed decreased levels of PPARgamma. We conclude that 15dPGJ2 modulates placental lipid metabolism and NO production. The concentration and function of 15dPGJ2 and concentrations of PPARgamma were altered in placentas from diabetic rats, anomalies probably involved in diabetes-induced placental dysfunction.