Abstract

Introduction: Placental fatty acid transfer is critical to meet the fetal requirements for biosynthesis of biological membranes, myelin and various signaling molecules. Increasing evidence suggests that the direction and magnitude of fatty acid flux is mainly determined by the availability of transfer proteins (Dutta-Roy, 2000). However, the relative expression of these proteins in human placental tissue is not known. The aim of this study was to elucidate the human placental mRNA expression of proteins that may regulate placental fatty acid transfer. Methods: We collected placental tissue from five pregnant women undergoing caesarean section at 38+/−1.1 weeks of gestation and from five different placenta locations. We quantified the fatty acid composition at the individual locations by gas-liquid chromatography (Klingler et al., 2003) and mRNA expression of placental fatty acid transport proteins-1 (FATP-1) and −4 (FATP-4), heart-fatty acid binding protein (H-FABP) and liver-FABP (L-FABP) by real time-PCR. The mRNA expression of these proteins was expressed relative to that of the house keeping gene beta-2-microglobulin. Results: The mRNA expression of plasma membrane proteins FATP-1 and FATP-4 (39.5+/−6.4a, and 16.4+/−2.8b) was significantly higher than that of the cytosolic proteins H-FABP (9.3+/−0.7c) and L-FABP. The expression of L-FABP was too low in placenta for accurate quantification. No significant differences were detected in the expression of FATP-1, FATP-4 and H-FABP between the different placental locations. Conclusion: Our results indicate the feasibility of reproducible quantification of placental mRNA expression of some fatty acid transport proteins and provide first results on their expression in human placentas at term. Although a higher expression of membrane bound transport proteins than of cytosolic transport proteins was demonstrated, further studies are needed to establish the role of the individual placental proteins in the fetal accretion of fatty acids and their response to maternal diet and disease.

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