Department of Obstetrics and Gynecology, University Hospital of Northern Norway and Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway.
Reprod Sci. 2009 Jul;16(7):701-11. doi: 10.1177/1933719109334256. Epub 2009 Apr 16.
We evaluated global placental gene expression in intrauterine growth restriction (IUGR; n = 8) compared to normal pregnancies (n = 8) and studied possible additional effect of preeclampsia. Placental samples were collected from IUGR pregnancies due to placental insufficiency ascertained by hemodynamic studies. Four IUGR pregnancies were associated with preeclampsia. Gene expression profile was evaluated by 30k oligonucleotide microarrays. Principal component analysis (PCA) showed good separation in terms of gene expression patterns between the groups. Pathway analysis showed upregulation of inflammation mediated by chemokine and cytokine signaling pathway in the IUGR placentas. Genes involved in placental glucocorticoid metabolism were also differentially expressed. None of the known imprinted placental genes were differentially expressed. Subgroup analysis between IUGR placentas with and without preeclampsia showed few (n = 27) differentially expressed genes. In conclusion, IUGR due to placental insufficiency appears to alter placental glucocorticoid metabolism, upregulates inflammatory response in placenta, and shares common pathogenic mechanisms with severe early-onset preeclampsia.
我们评估了宫内生长受限(IUGR;n=8)与正常妊娠(n=8)的胎盘基因表达情况,并研究了子痫前期的可能附加影响。由于通过血液动力学研究确定胎盘功能不全,从 IUGR 妊娠中采集了胎盘样本。4 例 IUGR 妊娠与子痫前期相关。通过 30k 寡核苷酸微阵列评估基因表达谱。主成分分析(PCA)表明,各组之间的基因表达模式有很好的分离。途径分析表明,IUGR 胎盘中的趋化因子和细胞因子信号通路介导的炎症反应上调。参与胎盘糖皮质激素代谢的基因也表现出差异表达。已知的印迹胎盘基因没有差异表达。有无子痫前期的 IUGR 胎盘的亚组分析显示,差异表达的基因很少(n=27)。总之,由于胎盘功能不全导致的 IUGR 似乎改变了胎盘糖皮质激素代谢,上调了胎盘的炎症反应,并与严重的早发型子痫前期具有共同的发病机制。