Placental expression of lipoprotein lipase (LPL), endothelial lipase (EL) and hormone sensitive lipase (HSL) is decreased in pregnancies complicated by preeclampsia (PE)

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 498-514-Female Reproductive Endocrinology
Basic/Translational
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-508
Helen L. Barrett*1, Harold David McIntyre2, Kerina J Denny1, Trent Woodruff1, Leonie K Callaway3 and Marloes Dekker Nitert3
1The University of Queensland, Australia, 2Mater Health Services, S Brisbane QLD, Australia, 3The University of Queensland, Herston, Australia
Preeclampsia (PE) is associated with maternal and neonatal morbidity and mortality. In PE, the normal hyperlipidemia of pregnancy is exaggerated, with markedly increased maternal hypertriglyceridemia, with higher VLDL1 and VLDL2 concentrations [1]. There is also a rise in free fatty acids concentrations above normal pregnancy levels. This excessive increase in maternal lipids is thought to contribute to endothelial dysfunction [2, 3]. Placental lipases such as lipoprotein lipase (LPL), endothelial lipase (EL) and hormone-sensitive lipase (HSL) are involved in transferring lipids from mother to fetus. The purpose of this study was to examine the expression of LPL, EL and HSL in pregnancies complicated by late onset PE. Placentas from 20 women with PE and 21 uncomplicated pregnancies, matched for maternal prepregnancy BMI and gestational age of delivery were collected with informed consent. RNA was extracted and reverse transcribed. Gene expression levels for LPL, EL and HSL were determined with real time PCR and analysed with the ΔΔCt method. Lipase expression was normalised to expression of ß-actin, desmin (smooth muscle cells), cytokeratin 7 (trophoblasts) and CD34 (endothelial cells) using the geometric mean. Data were analyzed using Mann-Whitney U tests. Placental localization of LPL, EL and HSL was determined with immunohistochemistry. There was no difference in maternal prepregnancy BMI (PE: 26.8 ± 1.3 kg/m2 (mean±SE) vs. controls: 30.0 ± 1.44 kg/m2), birth centile (PE: 42.3 ± 7.3 vs. controls: 48.8 ± 7.7), or gestational age of delivery (PE: 37.7 ± 0.6 weeks vs. controls: 38.5 ± 0.3 weeks). Expression of LPL (PE: 0.38 ± 0.09 vs. control 2.47 ± 0.91, P=0.0001), EL (PE: 0.25 ± 0.14 vs. control 1.64 ± 0.36, P <0.0001) and HSL (PE: 1.31 ± 0.98 vs. control 1.64 ± 0.31, P = 0.0001) were reduced in placentas from pregnancies complicated by PE. LPL and EL localized to trophoblasts and endothelial cells, whereas HSL expression was limited to trophoblasts. These results suggest that PE is associated with decreased expression of lipases in the placenta. Decreased expression may reflect reduced lipid transfer across the placenta. An analysis of protein levels is underway.

1.            Sattar N, et al., Obstet Gynecol 1997, 89(3):403-408. 2.            Adiga U,et al., J Chin Med Assoc 2007, 70(10):435-438. 3.            Bayhan G,et al., Gynecological Endocrinology 2005, 21(1):1-6.

Nothing to Disclose: HLB, HDM, KJD, TW, LKC, MD

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: Pfizer Australia, Cardiovascular Lipid Research Grant; Royal Brisbane and Women's Hospital Foundation