Gauster M, Hiden U, Blaschitz A, Frank S, Lang U, Alvino G, Cetin I, Desoye G, Wadsack C
Institute of Histology, Cell Biology, and Embryology, Center of Molecular Medicine, Medical University of Graz, Harrachgasse 21/VII, Graz, Austria.
J Clin Endocrinol Metab. 2007 Jun;92(6):2256-63. doi: 10.1210/jc.2006-2403. Epub 2007 Mar 13.
Fetal supply of maternally derived fatty acids requires lipase-mediated hydrolysis of lipoprotein-borne triglycerides and phospholipids at the placental surface.
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.
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 included women with uncomplicated pregnancies and pregnancies complicated by IUGR.
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.
EL is the predominant TLG family member in the human placenta present at both interfaces. EL and LPL are dysregulated in IUGR.
胎儿获取母体来源的脂肪酸需要胎盘表面的脂肪酶介导脂蛋白携带的甘油三酯和磷脂的水解。
本研究的目的是检验以下假设：甘油三酯脂肪酶基因（TLG）家族成员在人胎盘的母胎（合体滋养层）和胎儿胎盘（内皮细胞）界面表达，且其表达在妊娠病理状态下会发生改变。
通过微阵列、逆转录聚合酶链反应（RT-PCR）、蛋白质免疫印迹和免疫组织化学分析TLG家族成员在人早孕和足月胎盘的原代胎盘细胞（滋养层细胞和内皮细胞）及组织中的表达。比较正常妊娠和合并宫内生长受限（IUGR）妊娠中它们的表达情况。
参与者包括正常妊娠妇女和合并IUGR的妊娠妇女。
内皮脂肪酶（EL）和脂蛋白脂肪酶（LPL）是TLG家族中仅在人胎盘关键细胞中表达的脂肪酶。在孕早期，EL和LPL在滋养层细胞中表达。足月时，在滋养层细胞和内皮细胞中检测到EL，而这些细胞中未检测到LPL。在胎盘血管中均发现这两种脂肪酶，EL存在于血管内皮细胞中，LPL存在于周围平滑肌细胞中。在整个胎盘组织中，EL表达在孕早期和足月时占主导。与正常胎盘相比，IUGR胎盘组织中EL信使核糖核酸（mRNA）水平降低（30%；P<0.02），而LPL mRNA表达增加（2.4倍；P<0.015）。
EL是存在于两个界面的人胎盘中主要的TLG家族成员。EL和LPL在IUGR中表达失调。
