Feto-placental Unit: From Development to Function.

The placenta is an intriguing organ that allows us to survive intrauterine life. This essential organ connects both mother and fetus and plays a crucial role in maternal and fetal well-being. This chapter presents an overview of the morphological and functional aspects of human placental development. First, we describe early human placental development and the characterization of the cell types found in the human placenta. Second, the human placenta from the second trimester to the term of gestation is reviewed, focusing on the morphology and specific pathologies that affect the placenta. Finally, we focus on the placenta's primary functions, such as oxygen and nutrient transport, and their importance for placental development.

The LDL receptor: Traffic and function in trophoblast cells under normal and pathological conditions.

During pregnancy, the developing foetus requires large amounts of cholesterol from the maternal plasma, which is mediated by proteins such as the receptor for low-density lipoproteins (LDLR). The quantity of LDLR available in the syncytiotrophoblast plasma membrane is an important factor for the uptake, metabolism, and transfer of cholesterol to foetal circulation. Because of the relevance of this receptor for cellular and systemic cholesterol metabolism in non-placental cells, the study of mechanisms associated with LDLR trafficking, such as the availability in the cell membrane, endocytosis, recycling, sorting, and degradation, have been extensively studied. Multiple protein groups are required for proper LDL/LDLR trafficking. Changes in the function of these proteins are related to hypercholesterolemia, the main risk factor associated with cardiovascular disease. It is well known that the placenta plays an essential role as a barrier between maternal lipids and the foetus and that imbalances in maternal cholesterol levels during pregnancy are frequent and associated with cardiovascular disease in the offspring. However, there is little information regarding lipoprotein trafficking in this system. In this review, we summarize the available information on LDLR trafficking, emphasizing the few reports related to receptor biology in placental cells from normal and pathological pregnancies. We conclude that extensive research on the cell biology of the placenta is required to unravel the endocytic trafficking of proteins such as LDLR in a highly specialized cell such as the syncytiotrophoblast.

Syncytiotrophoblast stress in early onset preeclampsia: The issues perpetuating the syndrome.

Preeclampsia is a pregnancy-specific syndrome characterized by a sudden increase in blood pressure accompanied by proteinuria and/or maternal multi-system damage associated to poor fetal outcome. In early-onset preeclampsia, utero-placental perfusion is altered, causing constant and progressive damage to the syncytiotrophoblast, generating syncytiotrophoblast stress. The latter leads to the detachment and release of syncytiotrophoblast fragments, anti-angiogenic factors and pro-inflammatory molecules into maternal circulation, resulting in the emergence and persistence of the characteristic symptoms of this syndrome during pregnancy. Therefore, understanding the origin and consequences of syncytiotrophoblast stress in preeclampsia is vital to develop new therapeutic alternatives, focused on reducing the burden of this syndrome. In this review, we describe five central characteristics of syncytial stress that should be targeted or prevented in order to reduce preeclampsia symptoms: histological alterations, syncytiotrophoblast damage, antiangiogenic protein export, placental deportation, and altered syncytiotrophoblast turnover. Therapeutic management of these characteristics may improve maternal and fetal outcomes.