Fibrin-type Fibrinoid in Placentae from Pregnancies Associated with Maternal Smoking: Association with Villous Trophoblast and Impact on Intervillous Porosity

Mayhew, T.M.; Brotherton, L.; Holliday, Ebony; Orme, G.; Bush, Peter G.

doi:10.1053/plac.2002.0943

Cited by 24 publications

(8 citation statements)

References 69 publications

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“…The study of glycosis blockage caused STB degeneration and immediately followed by blood clot at the trophoblast surface (Kaufmann et al). The increased accumulation of Fd at denudation site of placenta was also reported in smoker (Mayhew et al, 2003). From our results, we suggested that the increased Fd probably occurred to replace the injury site after STB apoptosis.…”

Section: Discussionsupporting

confidence: 82%

Increasing of Syncytial Knot and Fibrinoid Deposit in High-Cd Accumulated Human Placentas

et al. 2013

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SUMMARY:A toxic metal, cadmium (Cd), can accumulate in human organs. Placenta is usually used as indicator organ for Cd exposure. Therefore, we aim to investigate the different of placental morphology between the low-and high-Cd accumulated placentas. The samples were collected from 14 pregnant women who resided in low-Cd contaminated (L-Cd group) and high-Cd contaminated (HCd group) areas. The concentrations of Cd in blood (B-Cd), urine (U-Cd) and placentas (P-Cd) were measured by ICP-MS and AAS. The morphological appearance of placentas was examined by using routine paraffin section and H & E staining. The results showed that levels of B-Cd, U-Cd and P-Cd were significantly higher in H-Cd group than in L-Cd group (p= 0.001). Moreover, the B-Cd was positively correlated with U-Cd (rs= 0.823, p= 0.000) and P-Cd concentrations (rs= 0.854, p= 0.000). The appearances of syncytial knot (STK) and fibrinoid deposit (Fd) were obviously greater in H-Cd group than in L-Cd group (p= 0.007, p= 0.026). The STK was positively correlated with both Fd (rs= 0.572, p= 0.032) and P-Cd concentration (rs= 0.766, p= 0.001). Although the chorioamnitis and decidual inflammation features were found in both groups but the appearance in H-Cd group seems to be more severe than in L-Cd group. From these results, we suggested that high Cd level in placenta may be involved in morphological changes, especially STK and Fd increasing and probably disturb the connection between maternal and fetal circulation.

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Section: Discussionsupporting

confidence: 82%

Increasing of Syncytial Knot and Fibrinoid Deposit in High-Cd Accumulated Human Placentas

et al. 2013

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“…Upon STB denudation, however, CD36 and CS-A were in direct contact with iRBC-containing maternal blood. Although we do not know why P. falciparuminfected placentas display this lesion, it has been noted in other pregnancy complications [41,63], and there is evidence that inflammation may be a cause. For example, in vitro experiments demonstrated that monocyte adhesion to syncytium and concomitant production of tissue necrosis factor alpha (TNF-a) promoted STB loss [64].…”

Section: Discussionmentioning

confidence: 84%

Histopathologies, Immunolocalization, and a Glycan Binding Screen Provide Insights into Plasmodium falciparum Interactions with the Human Placenta

Hromatka¹,

Ngeleza²,

Adibi³

et al. 2013

Biology of Reproduction

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During pregnancy, Plasmodium falciparum-infected erythrocytes cytoadhere to the placenta. Infection is likely initiated at two sites where placental trophoblasts contact maternal blood: 1) via syncytiotrophoblast (STB), a multicellular transporting and biosynthetic layer that forms the surface of chorionic villi and lines the intervillous space, and 2) through invasive cytotrophoblasts, which line uterine vessels that divert blood to the placenta. Here, we investigated mechanisms of infected erythrocyte sequestration in relationship to the microanatomy of the maternal-fetal interface. Histological analyses revealed STB denudation in placental malaria, which brought the stromal cores of villi in direct contact with maternal blood. STB denudation was associated with hemozoin deposition (P = 0.01) and leukocyte infiltration (P = 0.001) and appeared to be a feature of chronic placental malaria. Immunolocalization of infected red blood cell receptors (CD36, ICAM1/CD54, and chondroitin sulfate A) in placentas from uncomplicated pregnancies showed that STB did not stain, while the underlying villous stroma was immunopositive. Invasive cytotrophoblasts expressed ICAM1. In malaria, STB denudation exposed CD36 and chondroitin sulfate A in the villous cores to maternal blood, and STB expressed ICAM1. Finally, we investigated infected erythrocyte adherence to novel receptors by screening an array of 377 glycans. Infected erythrocytes bound Lewis antigens that immunolocalized to STB. Our results suggest that P. falciparum interactions with STB-associated Lewis antigens could initiate placental malaria. Subsequent pathologies, which expose CD36, ICAM1, and chondroitin sulfate A, might propagate the infection.

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“…In the present study, vessel lengths were affected in a dose-dependent manner, with PATHOLOGICAL EFFECTS OF ANGIOSTATIN 4.5 511 both 1 and 10 mg/kg AS 4.5 leading to a ;2-fold increase in placental fetal vascular length, whereas 20 mg/kg AS 4.5 was associated with a catastrophic 71% decline in total length, which may be partially compensated by increases in total maternal labyrinthine blood space length. A higher ratio of maternal/fetoplacental vascular volumes is also implicit in morphometric data obtained from human placentas associated with FGR [51]. The effects of a single dose of angiostatin on chorioallantoic membrane vascularization in 7-day-old quail embryos revealed a decrease in vascular growth by a maximum of 68% compared to that in control embryos [52].…”

Section: Discussionmentioning

confidence: 94%

Thrombophilic-Type Placental Pathologies and Skeletal Growth Delay Following Maternal Administration of Angiostatin4.5 in Mice

Atkinson

Mukhopadhyay

Jiang

et al. 2011

Biology of Reproduction

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During placentation, the concentration of fibrinous deposits on the surfaces of maternal vasculature plays a role in villous development and has been strongly implicated in the pathophysiology of human fetal growth restriction (FGR). Fibrinous deposits are conspicuous sites of platelet aggregation where there is local activation of the hemostatic cascade. During activation of the hemostatic cascade, a number of pro- and antiangiogenic agents may be generated at the cell surface, and an imbalance in these factors may contribute to the placental pathology characteristic of FGR. We tested the hypothesis that angiostatin(4.5) (AS(4.5)), a cleavage fragment of plasminogen liberated at the cell surface, is capable of causing FGR in mice. Increased maternal levels of AS(4.5) in vivo result in reproducible placental pathology, including an altered vascular compartment (both in decidual and labyrinthine layers) and increased apoptosis throughout the placenta. In addition, there is significant skeletal growth delay and conspicuous edema in fetuses from mothers that received AS(4.5). Maternally generated AS(4.5), therefore, can access maternal placental vasculature and have a severe effect on placental architecture and inhibit fetal development in vivo. These findings strongly support the hypothesis that maternal AS(4.5) levels can influence placental development, possibly by directly influencing trophoblast turnover in the placenta, and contribute to fetal growth delay in mice.

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Fibrin-type Fibrinoid in Placentae from Pregnancies Associated with Maternal Smoking: Association with Villous Trophoblast and Impact on Intervillous Porosity

Cited by 24 publications

References 69 publications

Increasing of Syncytial Knot and Fibrinoid Deposit in High-Cd Accumulated Human Placentas

Increasing of Syncytial Knot and Fibrinoid Deposit in High-Cd Accumulated Human Placentas

Histopathologies, Immunolocalization, and a Glycan Binding Screen Provide Insights into Plasmodium falciparum Interactions with the Human Placenta

Thrombophilic-Type Placental Pathologies and Skeletal Growth Delay Following Maternal Administration of Angiostatin4.5 in Mice

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