لخّصلي

Mother, fetus and placenta, this trio constitutes the functional equilibrium during the perinatal period.Shallow cytotrophoblast migration towards uterine spiral arterioles leads to inadequate vascular remodeling and a hypoperfused placenta, marking the first stage of preeclampsia.in anchoring villi, cytotrophoblast also fuse, they aggregate into columns of mononuclear cells that attach to and then invade the decidualized endometrium and the first third of the myometrium (interstitial invasion), as well as the associated portions of uterine (spiral) arterioles (endovascular invasion).The transformation of uterine spiral arteries leads to the creation of a low-resistance arterial network, facilitating a substantial increase in blood flow to meet the metabolic demands of the developing uteroplacental unit.Cell migration, including trophoblast invasion, relies significantly on adhering to extracellular matrix proteins for anchoring and traction.

Mother, fetus and placenta, this trio constitutes the functional equilibrium during the perinatal period. Any defect in one of them puts the other at risk, as the case in preeclampsia, which occurs as a result of a defect in the placenta. so the observation of the morphological features of placentae both in normal pregnancy and preeclampsia must be taken into consideration. Normal placentation relies on differentiation of its specialized epithelial cells, known as trophoblasts . Human cytotrophoblast stem cells follow one of two differentiation pathways. Those in floating villi detach from their basement membrane and fuse to form a syncytial layer that is in direct contact with maternal blood. These syncytiotrophoblasts play an important role in nutrient, waste and gas exchange. in anchoring villi, cytotrophoblast also fuse, they aggregate into columns of mononuclear cells that attach to and then invade the decidualized endometrium and the first third of the myometrium (interstitial invasion), as well as the associated portions of uterine (spiral) arterioles (endovascular invasion). Cytotrophoblast invasion ensures proper anchoring and supporting of the fetus to the mother and creates the large-diameter, low-resistance vessels that carry blood to the floating villi which are important for the exchange of substances between mother and fetus during pregnancy. The transformation of uterine spiral arteries leads to the creation of a low-resistance arterial network, facilitating a substantial increase in blood flow to meet the metabolic demands of the developing uteroplacental unit. Cell migration, including trophoblast invasion, relies significantly on adhering to extracellular matrix proteins for anchoring and traction. This is facilitated by surface receptors known as adhesion molecules, like integrins. Integrins are transmembrane glycoproteins comprising noncovalently linked alpha and beta subunits. The transition of trophoblast cells to an invasive phenotype involves altering their integrin expression pattern, allowing them to effectively penetrate maternal tissues during placental development. In preeclampsia, this remodeling process doesn’t occur as it should. Shallow cytotrophoblast migration towards uterine spiral arterioles leads to inadequate vascular remodeling and a hypoperfused placenta, marking the first stage of preeclampsia.