Placental exosomes are described as released carriers of microribonucleic acids involved in fetal-maternal signaling. The review uses them to expand the concept of where the placental interface functionally resides.
First-pass extracted concept
placental exosomes
Aliases
exosomes carrying microribonucleic acids
Extracted Explainers
What the tool is doing
What problem it solves
What it does not solve
Evidence Snippets
Supporting Sources
Linked Claims
Extravillous trophoblast cells interact with maternal innate immune cells in the uterine wall, and these interactions are described as physiological rather than classical immunological and likely contribute to spiral artery remodeling.
Extravillous trophoblast cells migrate from the placenta into the uterine wall, in which they interact with cells of the maternal innate immune system. These interactions have a physiological, rather than a classical immunological, outcome and most probably mediate remodeling of the uterine spiral arteries that supply the placenta.
Endometrial glands provide histotrophic support during the first weeks of pregnancy, and the placenta appears able to stimulate its own development by up-regulating gland activity in response to endocrine signals.
The endometrial glands provide histotrophic support during the first weeks of pregnancy, and the placenta appears able to stimulate its own development by up-regulating gland activity in response to endocrine signals.
The placenta performs multiple fetal support functions analogous to lungs, gut, kidneys, and liver during pregnancy and also exerts major endocrine effects on maternal physiology and metabolism.
During the course of a pregnancy, it acts as the lungs, gut, kidneys, and liver of the fetus. The placenta also has major endocrine actions that modulate maternal physiology and metabolism
Deported aggregates of transcriptionally active trophoblast nuclei and exosomes carrying microribonucleic acids are presented as mechanisms that challenge traditional definitions of fetal-maternal signaling and the placental interface.
Furthermore, deportation of aggregates of transcriptionally active trophoblast nuclei, and the release of exosomes carrying microribonucleic acids challenge our perceptions of fetal-maternal signaling and where the placental interface actually lies.