Barrett Helen L, Kubala Marta H, Scholz Romero Katherin, Denny Kerina J, Woodruff Trent M, McIntyre H David, Callaway Leonie K, Dekker Nitert Marloes
UQ Centre for Clinical Research, The University of Queensland, Herston, QLD, Australia.
Obstetric Medicine, Royal Brisbane and Women's Hospital, Herston, QLD, Australia.
Reprod Biol Endocrinol. 2015 Sep 4;13:100. doi: 10.1186/s12958-015-0098-9.
Preeclampsia (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.
Placentae 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.
Gene 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.
These 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.
子痫前期（PE）与孕产妇及新生儿的发病和死亡相关。在子痫前期中，孕期生理性高脂血症会加剧。本研究的目的是检测脂肪甘油三酯脂肪酶（ATGL）、激素敏感性脂肪酶（HSL）、脂蛋白脂肪酶（LPL）和内皮脂肪酶（EL）在合并子痫前期的妊娠中的表达。
收集16例子痫前期患者及20例与子痫前期患者孕前BMI和分娩孕周相匹配的正常妊娠孕妇的胎盘。通过Q-PCR和蛋白质印迹法检测胎盘脂肪酶的基因和蛋白质表达。通过亚硫酸氢盐测序评估LPL启动子的DNA甲基化。分析脂肪酶的定位和活性。
子痫前期患者中所有脂肪酶的基因表达均显著降低，HSL蛋白水平也降低。在子痫前期和对照胎盘的滋养层细胞和内皮细胞中均发现所有脂肪酶。子痫前期胎盘与对照胎盘的LPL启动子甲基化无差异。子痫前期患者胎盘的脂肪酶活性未改变。
这些结果表明，与晚发型子痫前期相关的胎盘脂肪酶基因表达降低，但蛋白质表达或脂肪酶活性未降低，并非子痫前期脂质异常的主要原因。
