Pregnancy in placental mammals including the human starts with the process of implantation of the embryo followed by placental development. The placenta serves multiple functions essential for fetal growth and survival. The hemochorial type of placenta, such as in the human, is also a highly invasive tumor-like structure which invades the pregnant uterus and its vasculature to nourish the fetus. These functions are provided by two classes of trophoblast (villous and extravillous) cells. They originate from the bi-potent trophoblast stem cells (TSC) contained within the cytotrophoblast layer of the chorionic villi. Villous syncytiotrophoblast layer lining the maternal blood sinusoids arise from the TSC by cell fusion and are primarily engaged in absorptive, exchange and endocrine functions. Extravillous trophoblast (EVT) cells arise from the TSC as highly migratory cell columns, which proliferate at the villus base and invade the uterine decidua and spiral arteries (SA). They undergo endothelial-like (endovascular) differentiation to invade and remodel distal segments of the SA into low-resistance tubes that allow steady flow of maternal blood for fetal nourishment. Poor EVT invasion & SA remodeling are linked with maternal preeclampsia (PE) and fetal growth restriction (FGR). A large number of molecules produced locally at the fetal maternal interface either by the trophoblast or various maternal cell types within the endometrium or the decidua (decidual cells, immune cells, stromal cells), positively or negatively regulate trophoblast differentiation, proliferation, migration and invasion , and other pregnancy-related events such as decidual maturation, angiogenesis and lymphangiogenesis, maintaining a healthy utero-placental homeostasis.
Molecules responsible for uteroplacental homeostasis include a variety of growth factors, growth factor-binding proteins and proteoglycans, cytokines , chemokines lipid derivatives and matrix-degrading enzymes or their inhibitors. An altered production of some of these factors can lead to a variety of pregnancy related pathologies such as pregnancy loss, FGR, PE and hyper-invasive placentas (placenta acreta, increta and percreta). A good deal of information is already available on the functions of specific maternal or fetally-derived cells of the placenta and their products responsible for normal placental functions and their alterations in the pathogenesis of pregnancy-associated diseases. However there remains a large gap in the knowledge. The goal of the present research topis is to review specific areas of cellular/molecular interactions that contribute to normal pregnancy or pregnancy associated diseases and to identify gaps in the knowledge for future research to address.
Themes of interest for submissions include, but are not limited to:
- Roles of uterine natural killer cells in pregnancy and pregnancy failure
- Function of uterine macrophages and dendritic cells in immune protection of the fetus.
- Roles of prostaglandins and their receptors in pregnancy.
- Roles of decorin and decorin receptors in pregnancy.
- Roles of osteopontin in pregnancy
- Roles of hypoxia and hypoxia regulated pathways in pregnancy success and pregnancy-associated diseases
- Roles of angiogenic growth factors and their receptors in pregnancy
- Regulation of human trophoblast stem cells
- Roles of interleukins and chemokines in pregnancy
- Roles of inflammation in preeclampsia
- Epigenetic regulators of pregnancy success
- Roles of extracellular vesicles in fetal-maternal cross talk
- Roles of insulin-like growth factor and IGF-binding - proteins in fetal growth
- Control mechanisms in uterine arterial remodelling in normal pregnancy and pregnancy-related diseases
Pregnancy in placental mammals including the human starts with the process of implantation of the embryo followed by placental development. The placenta serves multiple functions essential for fetal growth and survival. The hemochorial type of placenta, such as in the human, is also a highly invasive tumor-like structure which invades the pregnant uterus and its vasculature to nourish the fetus. These functions are provided by two classes of trophoblast (villous and extravillous) cells. They originate from the bi-potent trophoblast stem cells (TSC) contained within the cytotrophoblast layer of the chorionic villi. Villous syncytiotrophoblast layer lining the maternal blood sinusoids arise from the TSC by cell fusion and are primarily engaged in absorptive, exchange and endocrine functions. Extravillous trophoblast (EVT) cells arise from the TSC as highly migratory cell columns, which proliferate at the villus base and invade the uterine decidua and spiral arteries (SA). They undergo endothelial-like (endovascular) differentiation to invade and remodel distal segments of the SA into low-resistance tubes that allow steady flow of maternal blood for fetal nourishment. Poor EVT invasion & SA remodeling are linked with maternal preeclampsia (PE) and fetal growth restriction (FGR). A large number of molecules produced locally at the fetal maternal interface either by the trophoblast or various maternal cell types within the endometrium or the decidua (decidual cells, immune cells, stromal cells), positively or negatively regulate trophoblast differentiation, proliferation, migration and invasion , and other pregnancy-related events such as decidual maturation, angiogenesis and lymphangiogenesis, maintaining a healthy utero-placental homeostasis.
Molecules responsible for uteroplacental homeostasis include a variety of growth factors, growth factor-binding proteins and proteoglycans, cytokines , chemokines lipid derivatives and matrix-degrading enzymes or their inhibitors. An altered production of some of these factors can lead to a variety of pregnancy related pathologies such as pregnancy loss, FGR, PE and hyper-invasive placentas (placenta acreta, increta and percreta). A good deal of information is already available on the functions of specific maternal or fetally-derived cells of the placenta and their products responsible for normal placental functions and their alterations in the pathogenesis of pregnancy-associated diseases. However there remains a large gap in the knowledge. The goal of the present research topis is to review specific areas of cellular/molecular interactions that contribute to normal pregnancy or pregnancy associated diseases and to identify gaps in the knowledge for future research to address.
Themes of interest for submissions include, but are not limited to:
- Roles of uterine natural killer cells in pregnancy and pregnancy failure
- Function of uterine macrophages and dendritic cells in immune protection of the fetus.
- Roles of prostaglandins and their receptors in pregnancy.
- Roles of decorin and decorin receptors in pregnancy.
- Roles of osteopontin in pregnancy
- Roles of hypoxia and hypoxia regulated pathways in pregnancy success and pregnancy-associated diseases
- Roles of angiogenic growth factors and their receptors in pregnancy
- Regulation of human trophoblast stem cells
- Roles of interleukins and chemokines in pregnancy
- Roles of inflammation in preeclampsia
- Epigenetic regulators of pregnancy success
- Roles of extracellular vesicles in fetal-maternal cross talk
- Roles of insulin-like growth factor and IGF-binding - proteins in fetal growth
- Control mechanisms in uterine arterial remodelling in normal pregnancy and pregnancy-related diseases