Asami-Miyagishi Reiko, Iseki Sachiko, Usui Mayumi, Uchida Koji, Kubo Harumi, Morita Ikuo
Department of Craniofacial Embryology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan.
Biochem Biophys Res Commun. 2004 Mar 5;315(2):497-501. doi: 10.1016/j.bbrc.2004.01.074.
Peroxisome proliferator-activated receptor (PPAR) gamma is a nuclear receptor known to regulate adipogenesis. Deletion of the PPARgamma gene in the mouse results in death by embryonic day 10.0 (E10.0) due to the failure of establishment of a labyrinth layer in the placenta, which suggests that PPARgamma is involved in trophoblast differentiation. To define PPARgamma function further in placental development, the expression and localization of the PPARgamma gene in the rat placenta was investigated. RT-PCR analysis shows the presence of PPARgamma mRNA in the placenta of day 11 of pregnancy (d11). The expression level is higher at d13 and then later decreased. Immunohistochemistry detects both PPARgamma and its putative intrinsic ligand, 15-deoxy-Delta(12,14)-prostaglandin J(2), in the trophoblast of layer I which lined the maternal sinus. Oral administration of troglitazone, an agonist of PPARgamma, to pregnant rats between d9 and d11 increases the expression level of PPARgamma in the placenta and reduces the mortality of the fetuses by half. These results suggest that PPARgamma is required not only for trophoblast differentiation but also trophoblast maturation to establish maternal-fetal transport.
过氧化物酶体增殖物激活受体（PPAR）γ是一种已知可调节脂肪生成的核受体。小鼠中PPARγ基因的缺失会导致在胚胎第10.0天（E10.0）死亡，原因是胎盘迷路层无法形成，这表明PPARγ参与滋养层细胞分化。为了进一步明确PPARγ在胎盘发育中的功能，研究了PPARγ基因在大鼠胎盘中的表达和定位。逆转录聚合酶链反应（RT-PCR）分析显示，妊娠第11天（d11）的胎盘存在PPARγ信使核糖核酸（mRNA）。在d13时表达水平较高，随后下降。免疫组织化学检测到PPARγ及其假定的内源性配体15-脱氧-Δ（12,14）-前列腺素J2在衬于母体血窦的I层滋养层细胞中均有表达。在d9至d11期间给怀孕大鼠口服罗格列酮（一种PPARγ激动剂），可增加胎盘中PPARγ的表达水平，并使胎儿死亡率降低一半。这些结果表明，PPARγ不仅是滋养层细胞分化所必需的，也是建立母胎转运的滋养层细胞成熟所必需的。
