Maternal IL-11Rα function is required for normal decidua and fetoplacental development in mice
Maternal IL-11Rα function is required for normal decidua and fetoplacental development in mice
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DOI：
10.1101/gad.12.14.2234
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发表时间：
1998-07-15
影响因子：
10.5
通讯作者：
Gossler, A
中科院分区：
文献类型：
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作者：
Bilinski, P;Roopenian, D;Gossler, A
在真兽目哺乳动物中，绒毛膜尿囊胎盘的着床和建立对于胚胎的发育和存活是必不可少的。作为母体对着床的反应，子宫基质细胞增殖、分化并产生蜕膜，其包裹孕体并形成胎盘的母体部分。关于蜕膜的功能和调节其发育和维持的分子相互作用知之甚少。在这里，我们表明，受体远细胞因子白细胞介素-11（IL-11 R α）是所需的特定的正常建立的蜕膜。低型IL-11 R α等位基因纯合子的雌性是可育的，其囊胚植入并引起蜕膜反应。然而，由于细胞增殖减少，仅形成小的蜕膜。突变的蜕膜逐渐退化，因此胚胎来源的滋养层细胞产生滋养层巨细胞网络，但不能形成绒毛尿囊胎盘，表明蜕膜是正常胎儿胎盘形成所必需的。IL-11 R α在蜕膜以及许多其他组织和细胞类型中表达，包括卵巢和淋巴细胞。突变雌性中B和T淋巴细胞的分化状态和增殖反应是正常的，携带IL-11 R α突变卵巢的野生型雌性具有正常的蜕膜，这表明蜕膜化缺陷不会继发于淋巴器官或卵巢中干扰的IL-11 R α信号传导缺陷。着床部位的IL-11 R α信号传导似乎是蜕膜发育所需的。
In eutherian mammals, implantation and establishment of the chorioallantoic placenta are essential for embryo development and survival, As a maternal response to implantation, uterine stromal cells proliferate, differentiate, and generate the decidua, which encapsulates the conceptus and forms the maternal part of the placenta. Little is known about decidual functions and the molecular interactions that regulate its development and maintenance. Here we show that the receptor far the cytokine interleukin-11 (IL-11R alpha) is required specifically for normal establishment of the decidua. Females homozygous for a hypomorphic IL-11R alpha allele are fertile and their blastocysts implant and elicit the decidual response. Because of reduced cell proliferation, however, only small deciduae form. Mutant deciduae degenerate progressively, and consequently embryo-derived trophoblast cells generate a network of trophoblast giant cells but fail to form a chorioallantoic placenta, indicating that the decidua is essential for normal fetoplacentation. IL-11R alpha is expressed in the decidua as well as in numerous other tissues and cell types, including the ovary and lymphocytes. The differentiation state and proliferative responses of B and T-lymphocytes in mutant females were normal, and wild-type females carrying IL-11R alpha mutant ovaries had normal deciduae, suggesting that the decidualization defects do not arise secondarily as a consequence of perturbed IL-11R alpha signaling defects in lymphoid organs or in the ovary, Therefore, IL-11R alpha signaling at the implantation site appears to be required for decidua development.