Objectives: Human and animal studies have demonstrated that peroxisome proliferator-activated receptors (PPARs) are important in placental development and play key roles in metabolism and inflammation. We studied placental PPARδ, PPARγ, and retinoid X receptor α (RXRα) expression in healthy pregnancy and in preeclampsia (PET) and intrauterine growth restriction (IUGR).
Methods And Results: Using immunocytochemistry, PPARδ, PPARγ, and
RXRα
were localized to the cyto- and syncytiotrophoblast and invading trophoblast columns in first and second trimester placentas. Third trimester placentas from healthy pregnancy, and in PET and IUGR, demonstrated PPARδ, PPARγ, and RXRα staining within the syncytium, and localization within isolated cells in the stroma. In uncomplicated pregnancies, PPARδ mRNA expression (PPARδ:18s ratio, third trimester median 0.43 finterquartile (IQ) range 0.26-0.52] vs first trimester 0.20 [0.00-0.26], P = .03) and PPARδ protein expression (third trimester 3.94 [2.45-4. 68] vs first trimester 1.29 [0. 78-2.29] optical densitometry [OD] mm2
, P = .04) were higher in the third trimester than in the first trimester. There were no consistent differences in PPARδ, PPARγ, or RXRα mRNA and protein expression among PET or IUGR placentas and controls.
Conclusion: PPARδ expression is up-regulated between the first and third trimester, indicating a role for this nuclear receptor in placental function. Wefound no evidence that placental PPARδ, PPARγ, and RXRα expression is changed in PET or IUGR. This suggests that changes in total placental PPAR expression are not involved in the pathophysiology of these conditions.