Expression of PPAR and RXR isoforms in the developing rat and human term placentas

Placental fatty acid transfer is critical to meet the foetal requirements necessary for the biosynthesis of biological membranes, myelin, and various signaling molecules. The primary objective of this research was to elucidate the placental expression patterns of genes that may potentially regulate placental fatty acid transfer and homeostasis. In this study, we have elucidated the temporal and spatial patterns of expression of peroxisome proliferator-activated receptor (PPAR) and 9-cis retinoic acid receptor (RXR) isoforms in the junctional and labyrinth zones of the developing rat chorioallantoic placenta and in human term placenta. PPAR (alpha, beta, and gamma) and RXR (alpha, beta, and gamma) isoforms are nuclear hormone receptors that arc known to regulate gene transcription and protein expression levels of fatty acid transport and metabolism mediating proteins through the formation of a DNA binding heterodimer complex. In the present study, the expression patterns of PPAR and RXR isoforms were determined in developing rat placenta and human term placenta using RT-PCR and immunohistochemical analyses. PPARalpha, beta, gamma, RXRalpha, beta and gamma were expressed in both junctional (invasive/endocrine function) and labyrinth (transport barrier) zones of the rat placenta, from day 13 to day 21 of gestation. In the human term placenta, PPARalpha, beta, gamma, RXRalpha and gamma were observed, while RXRbeta was not detected. Immunocytochemistry staining results determined the presence of PPARalpha, beta, gamma, RXRalpha and gamma to be specific to the syncytial trophoblast layer of the human chorionic villi. The presence of PPAR and RXR isoforms in both the rat and human placentas suggest that PPAR and RXR isoforms are potential regulators of placental lipid transfer and homeostasis. Our work provides a framework for the further investigation of PPAR and RXR isoform specific regulation of placental fatty acid uptake, transport and metabolism. (C) 2002 Elsevier Science Ltd. All rights reserved.