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Dysregulation of Placental Endothelial Lipase and Lipoprotein Lipase in Intrauterine Growth-Restricted Pregnancies

Clinic of Obstetrics and Gynecology (M.G., U.H., U.L., G.D., C.W.), Medical University of Graz, 8036 Graz, Austria; Institute of Cell Biology, Histology and Embryology (M.G., A.B.), Center of Molecular Medicine, and Institute of Molecular Biology and Biochemistry (S.F.), Center of Molecular Medicine, Medical University of Graz, 8010 Graz, Austria; and Institute of Obstetrics and Gynecology (G.A., I.C.), Foundation Instituto di Ricovero e Cura a Carattere Scientifico Policlinico, Mangiagalli and Regina Elena, University of Milano, 20122 Milano, Italy

Address all correspondence and requests for reprints to: Martin Gauster, Institute of Histology, Cell Biology, and Embryology, Center of Molecular Medicine, Medical University of Graz, Harrachgasse 21/VII, 8010 Graz, Austria. E-mail: martin.gauster{at}meduni-graz.at.

Context: Fetal supply of maternally derived fatty acids requires lipase-mediated hydrolysis of lipoprotein-borne triglycerides and phospholipids at the placental surface.

Objective: The objective of the study was to test the hypothesis that members of the triglyceride lipase gene (TLG) family are expressed in the human placenta at the maternoplacental (syncytiotrophoblast) and fetoplacental (endothelial cells) interface and that their expression is altered in pregnancy pathologies.

Design and Setting: Expression of TLG family members in primary placental cells (trophoblast and endothelial cells) and tissues of first-trimester and term human placenta was analyzed by microarrays, RT-PCR, Western blotting, and immunohistochemistry. Their expression was compared between normal pregnancies and those complicated with intrauterine growth restriction (IUGR).

Participants: Participants included women with uncomplicated pregnancies and pregnancies complicated by IUGR.

Results: Endothelial lipase (EL) and lipoprotein lipase (LPL) were the only lipases among the TLG family expressed in key cells of the human placenta. In first trimester, EL and LPL were expressed in trophoblasts. At term, EL was detected in trophoblasts and endothelial cells, whereas LPL was absent in these cells. Both lipases were found at placental blood vessels, EL in vascular endothelial cells and LPL in the surrounding smooth muscle cells. In total placental tissue EL expression prevails in first trimester and at term. Compared with normal placentas, EL mRNA was decreased (30%; P < 0.02), whereas LPL mRNA expression was increased (2.4-fold; P < 0.015) in IUGR.

Conclusion: EL is the predominant TLG family member in the human placenta present at both interfaces. EL and LPL are dysregulated in IUGR.