Tranguch Susanne, Chakrabarty Anindita, Guo Yong, Wang Haibin, Dey Sudhansu K
Department of Cell & Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.
Biol Reprod. 2007 Sep;77(3):425-32. doi: 10.1095/biolreprod.107.062414. Epub 2007 May 30.
Reduced litter sizes in mice missing pentraxin 3 (Ptx3) have been attributed to fertilization failure. However, our global gene expression studies showed high uterine Ptx3 expression at the implantation site in mice, suggesting its role in blastocyst implantation. We initiated molecular and genetic studies in mice to explore the importance of uterine Ptx3 in this process. We found that Ptx3 is expressed in a unique and transient fashion at implantation sites. With the initiation of implantation on midnight of Day 4 of pregnancy, Ptx3 is expressed exclusively in stromal cells at the site of blastocysts. On Day 5, its expression is more intense in decidualizing stromal cells, but it disappears on Day 6. The expression again becomes evident in the deciduum on Day 7, followed by a more robust expression on Day 8, particularly at the antimesometrial pole. From Day 9, with the initiation of placentation, Ptx3 expression becomes undetectable. These results suggest a role for PTX3 in implantation and decidualization. Indeed, deletion of Ptx3 results in both compromised implantation and decidualization. Interleukin 1B (IL1B), a known inducer of Ptx3, is also transiently expressed in stromal cells at the implantation site, suggesting that IL1B is an inducer of uterine Ptx3 expression. In fact, uterine Ptx3 expression follows that of Il1b induced by lipopolysaccharide treatment on Day 7 of pregnancy. Collectively, these findings provide evidence for an important role for PTX3 in implantation and decidualization. This study has clinical implications, since PTX3 is expressed in the receptive endometrium, and trophoblast cells influence decidual Ptx3 expression in humans.
缺失五聚体蛋白3（Ptx3）的小鼠产仔数减少被归因于受精失败。然而，我们的全基因组表达研究显示，小鼠着床部位子宫中Ptx3表达水平很高，这表明其在胚泡着床过程中发挥作用。我们开展了小鼠分子和遗传学研究，以探究子宫Ptx3在此过程中的重要性。我们发现，Ptx3在着床部位以独特且短暂的方式表达。在妊娠第4天午夜着床开始时，Ptx3仅在胚泡着床部位的基质细胞中表达。在第5天，其在蜕膜化基质细胞中的表达更强，但在第6天消失。第7天，其在蜕膜中再次明显表达，随后在第8天表达更强烈，尤其是在反系膜极。从第9天开始，随着胎盘形成的开始，Ptx3表达无法检测到。这些结果表明PTX3在着床和蜕膜化过程中发挥作用。确实，Ptx3缺失会导致着床和蜕膜化均受损。白细胞介素1β（IL1B）是一种已知的Ptx3诱导剂，也在着床部位的基质细胞中短暂表达，这表明IL1B是子宫Ptx3表达的诱导剂。实际上，妊娠第7天经脂多糖处理诱导的子宫Ptx3表达与Il1b的表达一致。总的来说，这些发现为PTX3在着床和蜕膜化过程中的重要作用提供了证据。这项研究具有临床意义，因为PTX3在接受性子宫内膜中表达，并且滋养层细胞会影响人类蜕膜中Ptx3的表达。
