Limits...
Pathophysiology of placentation abnormalities in pregnancy-induced hypertension.

Furuya M, Ishida J, Aoki I, Fukamizu A - Vasc Health Risk Manag (2008)

Bottom Line: Several life-threatening diseases during pregnancy, such as pregnancy-induced hypertension (PIH) and eclampsia, are closely associated with placental dysfunction.For better understanding and effective therapeutic approaches to PIH, it is important to clarify pathological course of PIH-associated changes in the placenta.In addition, recent findings of vasoactive signalings in PIH and rodent PIH models are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa, Yokohama, Japan. mfuruya@yokohama-cu.ac.jp

ABSTRACT
During embryogenesis and development, the fetus obtains oxygen and nutrients from the mother through placental microcirculation. The placenta is a distinctive organ that develops and differentiates per se, and that organizes fetal growth and maternal condition in the entire course of gestation. Several life-threatening diseases during pregnancy, such as pregnancy-induced hypertension (PIH) and eclampsia, are closely associated with placental dysfunction. Genetic susceptibilities and poor placentation have been investigated intensively to understand the pathophysiology of PIH. It is currently thought that "poor placentation hypothesis", in which extravillous trophoblasts fail to invade sufficiently the placental bed, explains in part maternal predisposition to this disease. Cumulative studies have suggested that hypoxic micromilieu of fetoplacental site, shear stress of uteroplacental blood flow, and aberrantly secreted proinflammatory substances into maternal circulation synergistically contribute to the progression of PIH. For example, soluble form of vascular endothelial growth factor receptor-1 (sVEGFR-1) and soluble form of CD105 are elevated in circulation of PIH mothers. However, it remains to be poorly understood the pathological events in the placenta during the last half of gestation as maternal systemic disorders get worse. For better understanding and effective therapeutic approaches to PIH, it is important to clarify pathological course of PIH-associated changes in the placenta. In this review, current understanding of placental development and the pathophysiology of PIH placenta are summarized. In addition, recent findings of vasoactive signalings in PIH and rodent PIH models are discussed.

Show MeSH

Related in: MedlinePlus

Histology of the placenta in human (A) and mouse (B). The photo of whole layer of the placenta is shown in the left. High magnification of each layer is shown in the right.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2663465&req=5

f1-vhrm-4-1301: Histology of the placenta in human (A) and mouse (B). The photo of whole layer of the placenta is shown in the left. High magnification of each layer is shown in the right.

Mentions: Both in human and mouse, a normal term placenta is divided largely into three layers (Figures 1A, 1B): (1) Basal plate (maternal surface) and anchoring villi (most distal extensions of the primary stem villi) that interact directly with maternal endometrium. (2) Terminal villous unit (human) or labyrinth (mouse) where gas/nutrients exchange is taken place actively. (3) Chorionic plate (fetal surface) and stem villi that consist of dense connective tissue containing fetal vessels. Amnion and the underling chorion are membranes that cover chorionic plate, and the umbilical cord collects chorionic arteries and veins on chorionic plate generally in the center part (Kraus et al 2004).


Pathophysiology of placentation abnormalities in pregnancy-induced hypertension.

Furuya M, Ishida J, Aoki I, Fukamizu A - Vasc Health Risk Manag (2008)

Histology of the placenta in human (A) and mouse (B). The photo of whole layer of the placenta is shown in the left. High magnification of each layer is shown in the right.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2663465&req=5

f1-vhrm-4-1301: Histology of the placenta in human (A) and mouse (B). The photo of whole layer of the placenta is shown in the left. High magnification of each layer is shown in the right.
Mentions: Both in human and mouse, a normal term placenta is divided largely into three layers (Figures 1A, 1B): (1) Basal plate (maternal surface) and anchoring villi (most distal extensions of the primary stem villi) that interact directly with maternal endometrium. (2) Terminal villous unit (human) or labyrinth (mouse) where gas/nutrients exchange is taken place actively. (3) Chorionic plate (fetal surface) and stem villi that consist of dense connective tissue containing fetal vessels. Amnion and the underling chorion are membranes that cover chorionic plate, and the umbilical cord collects chorionic arteries and veins on chorionic plate generally in the center part (Kraus et al 2004).

Bottom Line: Several life-threatening diseases during pregnancy, such as pregnancy-induced hypertension (PIH) and eclampsia, are closely associated with placental dysfunction.For better understanding and effective therapeutic approaches to PIH, it is important to clarify pathological course of PIH-associated changes in the placenta.In addition, recent findings of vasoactive signalings in PIH and rodent PIH models are discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa, Yokohama, Japan. mfuruya@yokohama-cu.ac.jp

ABSTRACT
During embryogenesis and development, the fetus obtains oxygen and nutrients from the mother through placental microcirculation. The placenta is a distinctive organ that develops and differentiates per se, and that organizes fetal growth and maternal condition in the entire course of gestation. Several life-threatening diseases during pregnancy, such as pregnancy-induced hypertension (PIH) and eclampsia, are closely associated with placental dysfunction. Genetic susceptibilities and poor placentation have been investigated intensively to understand the pathophysiology of PIH. It is currently thought that "poor placentation hypothesis", in which extravillous trophoblasts fail to invade sufficiently the placental bed, explains in part maternal predisposition to this disease. Cumulative studies have suggested that hypoxic micromilieu of fetoplacental site, shear stress of uteroplacental blood flow, and aberrantly secreted proinflammatory substances into maternal circulation synergistically contribute to the progression of PIH. For example, soluble form of vascular endothelial growth factor receptor-1 (sVEGFR-1) and soluble form of CD105 are elevated in circulation of PIH mothers. However, it remains to be poorly understood the pathological events in the placenta during the last half of gestation as maternal systemic disorders get worse. For better understanding and effective therapeutic approaches to PIH, it is important to clarify pathological course of PIH-associated changes in the placenta. In this review, current understanding of placental development and the pathophysiology of PIH placenta are summarized. In addition, recent findings of vasoactive signalings in PIH and rodent PIH models are discussed.

Show MeSH
Related in: MedlinePlus