Bosco C, Díaz E, Gutiérrez R, González J, Parra-Cordero M, Rodrigo R, Barja P
Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
Anatomy and Developmental Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
Med Hypotheses. 2015 Jan;84(1):72-7. doi: 10.1016/j.mehy.2014.11.019. Epub 2014 Dec 3.
Preeclampsia (PE) is a major health problem occurring in pregnant women and the principal cause of maternal morbidity and perinatal mortality. It is characterized by alteration of the extravilli trophoblast cell migration toward the endometrial spiral arteries with a concomitant reduction in maternal blood flow in the placenta. This result in a state of ischemia-hypoxia which triggers an oxidative stress stage with production of reactive oxygen species. A cascade of cellular and molecular events leads then to endothelial dysfunction, transduction pathway signal disruption and induction of apoptosis and necrosis mechanisms and therefore a significant reduction in the amount of nutrients required for normal fetal development. Placental anchoring chorionic and stem villi present a skeleton of myofibroblasts arranged in parallel disposition to its longitudinal axis. The intraplacental blood volume is controlled by the contraction/relaxation of these myofibroblasts, promoting the delivery of nutrients and metabolites to the fetus. Recently, a new mesodermal originated cell type has been described in the villous stroma, the so named "telocytes". These cells are strategically located between the smooth muscle cells of the blood vessel wall and the myofibroblasts, and it is reasonable to hypothesize that they may play a pacemaker role, as in the intestine. This study provide new information supporting the notion that the occurrence of oxidative stress in PE is not only related to endothelial dysfunction and apoptosis of the trophoblast cells, but also involves telocytes and its putative role in the regulation of fetal blood flow and the intra-placental blood volume. Some ideas aimed at dilucidating the relationship between placental failure and the behavior of telocytes in pathological organs in adulthood, are also discussed.
子痫前期（PE）是发生在孕妇中的一个主要健康问题，也是孕产妇发病和围产期死亡的主要原因。其特征是绒毛外滋养层细胞向子宫内膜螺旋动脉的迁移发生改变，同时胎盘母体血流量减少。这导致缺血缺氧状态，引发氧化应激阶段并产生活性氧。一系列细胞和分子事件随后导致内皮功能障碍、信号转导通路破坏以及凋亡和坏死机制的诱导，从而使正常胎儿发育所需的营养物质数量显著减少。胎盘的锚定绒毛膜和主干绒毛呈现出成纤维细胞的骨架，这些成纤维细胞与其纵轴平行排列。胎盘内的血容量由这些成纤维细胞的收缩/舒张控制，促进营养物质和代谢产物向胎儿的输送。最近，在绒毛基质中描述了一种新的中胚层起源的细胞类型，即所谓的“间充质干细胞”。这些细胞战略性地位于血管壁平滑肌细胞和成纤维细胞之间，因此可以合理推测它们可能像在肠道中一样发挥起搏器的作用。本研究提供了新的信息，支持了以下观点：子痫前期中氧化应激的发生不仅与内皮功能障碍和滋养层细胞凋亡有关，还涉及间充质干细胞及其在调节胎儿血流和胎盘内血容量方面的假定作用。还讨论了一些旨在阐明胎盘功能衰竭与成年病理器官中间充质干细胞行为之间关系的观点。
