Molecular mechanisms underlying estrogen functions in trophoblastic cells. Focus on leptin expression

GAMBINO Y; MAYMÓ J; PÉREZ PÉREZ A; CALVO JC; SÁNCHEZ MARGALET V; VARONE C

PLACENTA

W B SAUNDERS CO LTD

Lugar: Londres; Año: 2011

0143-4004

Abstract: The steroid hormone 17â-estradiol (E2) is an estrogen that influences multiple aspects of placental function and fetal development in humans. During early pregnancy it plays a role in theregulation of blastocyst implantation, trophoblasts differentiation and invasiveness, remodeling ofuterine arteries, immunology and trophoblastic cells hormone production such as leptin.Estradiol exerts some effects through the action of classical estrogen receptors ERá and ERâ which act as ligand-activated transcription factors and regulate gene expression. In addition, E2 can elicit rapid responses from membrane-associated receptors, like activation of protein kinase pathways. Thus, the cellular effects of E2 will depend on the specific receptors expressed and the integration of their signaling events.Leptin, the 16000 MW protein product of the obese gene, was originally considered an adipocyte-derived signaling molecule for the central control of metabolism. However, pleiotropic effects of leptin have been identified in reproduction and pregnancy. The leptin gene is expressed in placenta, where leptin promotes proliferation and survival of trophoblastic cells. Expression of leptin in placenta is highly regulated by key pregnancy molecules as hCG and E2.The aim of this paper is to review the molecular mechanisms underlying estrogen functions introphoblastic cells; focusing on mechanisms involved in E2 regulation of placental leptin expression.