Moindjie Hadia, Santos Esther Dos, Gouesse Rita-Josiane, Swierkowski-Blanchard Nelly, Serazin Valérie, Barnea Eytan R, Vialard François, Dieudonné Marie-Noëlle
GIG-EA7404, Université de Versailles Saint-Quentin-en-Yvelines - Paris Saclay, Unité de Formation et de Recherche des Sciences de la Santé-Simone Veil, Montigny-le Bretonneux, France.
Service de Biologie Médicale, Centre Hospitalier de Poissy-Saint Germain, Poissy, France.
Cell Death Dis. 2016 Dec 1;7(12):e2504. doi: 10.1038/cddis.2016.382.
From the earliest stages of gestation, embryonic-maternal interaction has a key role in a successful pregnancy. Various factors present during gestation may significantly influence this type of juxta/paracrine interaction. PreImplantation Factor (PIF) is a recently identified factor with activity at the fetomaternal interface. PIF is secreted by viable embryos and directly controls placental development by increasing the invasive capacity of human extravillous trophoblasts (EVTs). To further specify PIF's role in the human placenta, we analyzed the genome-wide expression profile of the EVT in the presence of a synthetic PIF analog (sPIF). We found that sPIF exposure altered several pathways related to p53 signaling, survival and the immune response. Functional assays revealed that sPIF acts through the p53 pathway to reduce both early and late trophoblast apoptosis. More precisely, sPIF (i) decreases the phosphorylation of p53 at Ser-15, (ii) enhances the B-cell lymphoma-2 (BCL2) expression and (iii) reduces the BCL2-associated X protein (BAX) and BCL2 homologous antagonist killer (BAK) mRNA expression levels. Furthermore, invalidation experiments of TP53 allowed us to demonstrate that PIF's effects on placental apoptosis seemed to be essentially mediated by this gene. We have clearly shown that p53 and sPIF pathways could interact in human trophoblast and thus promotes cell survival. Furthermore, sPIF was found to regulate a gene network related to immune tolerance in the EVT, which emphasizes the beneficial effect of this peptide on the human placenta. Finally, the PIF protein levels in placentas from pregnancies affected by preeclampsia or intra-uterine growth restriction were significantly lower than in gestational age-matched control placentas. Taken as a whole, our results suggest that sPIF protects the EVT's functional status through a variety of mechanisms. Clinical application of sPIF in the treatment of disorders of early pregnancy can be envisioned.
从妊娠早期开始,胚胎与母体的相互作用对成功妊娠起着关键作用。妊娠期间存在的各种因素可能会显著影响这种旁分泌/自分泌相互作用。着床前因子(PIF)是最近发现的一种在母胎界面具有活性的因子。PIF由存活胚胎分泌,通过增强人绒毛外滋养层细胞(EVT)的侵袭能力直接控制胎盘发育。为了进一步明确PIF在人胎盘中的作用,我们分析了在合成PIF类似物(sPIF)存在的情况下EVT的全基因组表达谱。我们发现,暴露于sPIF会改变与p53信号传导、存活和免疫反应相关的几条途径。功能分析表明,sPIF通过p53途径发挥作用,减少早期和晚期滋养层细胞凋亡。更确切地说,sPIF(i)降低p53在Ser-15位点的磷酸化,(ii)增强B细胞淋巴瘤-2(BCL2)的表达,(iii)降低BCL2相关X蛋白(BAX)和BCL2同源拮抗剂杀手(BAK)的mRNA表达水平。此外,TP53的失活实验使我们能够证明PIF对胎盘细胞凋亡的影响似乎主要由该基因介导。我们清楚地表明,p53和sPIF途径可能在人滋养层细胞中相互作用,从而促进细胞存活。此外,发现sPIF调节与EVT免疫耐受相关的基因网络,这突出了这种肽对人胎盘的有益作用。最后,子痫前期或宫内生长受限妊娠的胎盘组织中PIF蛋白水平显著低于孕周匹配的对照胎盘。总体而言,我们的结果表明,sPIF通过多种机制保护EVT的功能状态。可以设想sPIF在治疗早期妊娠疾病中的临床应用。