Abstract
BackgroundPreeclampsia (PE) is associated with maternal and neonatal morbidity and mortality. In PE, the physiological hyperlipidaemia of pregnancy is exaggerated. The purpose of this study was to examine the expression of adipose triglyceride lipase (ATGL), hormone sensitive lipase (HSL), lipoprotein lipase (LPL) and endothelial lipase (EL) in pregnancies complicated by PE.MethodsPlacentae were collected from 16 women with PE and 20 women with uncomplicated pregnancies matched for maternal prepregnancy BMI and gestational age of delivery. Gene and protein expression of the placental lipases were measured by Q-PCR and Western blot. DNA methylation of the promoter of LPL was assessed by bisulfite sequencing. Lipase localisation and activity were analysed.ResultsGene expression of all lipases was significantly reduced, as was HSL protein level in women with PE. All lipases were localised to trophoblasts and endothelial cells in PE and control placentae. There was no difference in methylation of the LPL promoter between PE and control placentae. Lipase activity was not altered in placentae from women with PE.ConclusionThese results suggest that the decreased placental lipase gene but not protein expression or lipase activity, which is associated with late-onset PE is not a major contributor to the abnormal lipids seen in PE.
Highlights
Preeclampsia (PE) is associated with maternal and neonatal morbidity and mortality
There was no difference in localization between PE and control placentae for any of the four lipases described in this study, but we have demonstrated they are present in placental cells expected to be metabolically active
We have recently shown that adipose triglyceride lipase (ATGL) mRNA was increased and hormone sensitive lipase (HSL) mRNA decreased, with no difference in protein expression, in obese women with well controlled gestational diabetes mellitus compared to BMI matched controls [32]
Summary
Preeclampsia (PE) is associated with maternal and neonatal morbidity and mortality. In PE, most studies report exaggerated and early maternal gestational hyperlipidaemia [6,7,8], with marked hypertriglyceridemia, higher very low density lipoprotein (VLDL) concentrations [9] and higher levels of small, dense low density lipoprotein (LDL) [10]. There is a rise in maternal free fatty acid (FFA) concentrations above normal pregnancy levels [11]. This excessive increase in maternal lipids is thought to contribute to endothelial dysfunction, one of the hallmarks of PE [12, 13]. Women with a history of PE demonstrate persistent abnormalities in lipids postpartum [14, 15]
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