An ultrastructural and ultrahistochemical study of the human placenta in maternal pre-eclampsia

Jones, Carolyn J.P.; Fox, H.

doi:10.1016/s0143-4004(80)80016-6

Cited by 229 publications

(116 citation statements)

References 26 publications

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“…Along these lines, a major feature of the pathophysiology of PE is the failure of fetal trophoblasts to invade uterine arteries, resulting in reduced placental perfusion and ensued hypoxia/ ischemia. This localized oxygen and nutrient deprivation is associated with exaggerated trophoblast cell death (Jones & Fox 1980, Chua et al 1991, Knight et al 1998, Johansen et al 1999, Leung et al 2001, which has been suggested to directly contribute to the disease by releasing mediators of inflammation that promote endothelial activation and systemic maternal inflammation (Smarason et al 1993, Knight et al 1998, Redman & Sargent 2003. Although the etiology of PE is mostly unknown, a major hallmark is a generalized inflammatory response characterized by high cytokine levels, such as IL-1β, IL-6, IL-8 and tumor necrosis factor-α (Vince et al 1995, Mellembakken et al 2001, Laresgoiti-Servitje 2013, Harmon et al 2016.…”

Section: Preeclampsiamentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

219

161

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Inflammation is essential for successful embryo implantation, pregnancy maintenance and delivery. In the last decade, important advances have been made in regard to endogenous, and therefore non-infectious, initiators of inflammation, which can act through the same receptors as pathogens. These molecules are referred to as damage-associated molecular patterns (DAMPs), and their involvement in reproduction has only recently been unraveled. Even though inflammation is necessary for successful reproduction, untimely activation of inflammatory processes can have devastating effect on pregnancy outcomes. Many DAMPs, such as uric acid, high-mobility group box 1 (HMGB1), interleukin (IL)-1 and cell-free fetal DNA, have been associated with pregnancy complications, such as miscarriages, preeclampsia and preterm birth in preclinical models and in humans. However, the specific contribution of alarmins to these conditions is still under debate, as currently there is lack of information on their mechanism of action. In this review, we discuss the role of sterile inflammation in reproduction, including early implantation and pregnancy complications. Particularly, we focus on major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA (especially that of fetal origin) while giving an overview of the potential role of other candidate alarmins.Reproduction (2016) 152 R277-R292

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Section: Preeclampsiamentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

219

161

View full text Add to dashboard Cite

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“…There is decrease in synthetic activity of trophoblast and cellular respiration is also probably depressed. [22] PALP appears to be moderately resistant to hypoxia. Preeclamptic placentae showed considerable increase in lysosomal activity.…”

Section: Discussionmentioning

confidence: 93%

“…There is some evidence that compensatory changes which limit the effects of ischemic damage are brought into play in preeclampsia. [22] Since PALP has major role in transport and energy production increased PALP activity in preeclamptic placentae could be a compensatory mechanism to provide nutrition to the fetus in ischemic conditions.…”

Section: Discussionmentioning

confidence: 99%

Histochemistry of placental alkaline phosphatase in preeclampsia

Shevade

Arole

Paranjape

et al. 2016

Int J of Biomed & Adv Res

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Objectives: Placental alkaline phosphatase (PALP) is synthesized in placenta and increases with gestational age. Alkaline phosphatase supports pregnancy and could play an essential role in nutrient supply and growth of the fetus. Preeclampsia is a systemic disorder which affects 5 to 7 percent of women worldwide and is a major cause for maternal and neonatal morbidity and mortality. As it has a major role in fetal growth, nutrition and defense mechanism study of alkaline phosphatase enzymatic activity becomes essential. Methods: 50 normal and 50 preeclamptic placentae were collected immediately after delivery from Department of Obstetrics and Gynecology. Placentae were obtained from known preeclamptic consenting cases who had no history of hypertension before pregnancy or during first 20 weeks of gestation, who had consistently recorded systolic and diastolic blood pressure of 140 / 90 mm of Hg or above and proteinuria ≥ 300mg / 24 hrs. Alkaline phosphatase activity was demonstrated by using modified Gomori's method. Results: Intensity of PALP localization was stronger in preeclamptic placentae as compared to normotensive placentae. Conclusion: Placental ischemia is evident in preeclampsia. Uteroplacental insufficiency leads to increased syncytial damage in preeclamptic placentae which may lead to abnormally high PALP activity and consequent increase in serum alkaline phosphatase.

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“…Furthermore, in preeclampsia, endovascular invasion of the cytotrophoblast remains superficial and fails to undergo pseudovasculogenesis, due to severe failures of this cell compartment (Jones et al, 1980;Zhou et a., 1997). Therefore, the uterine blood vessels do not undergo adequate vascular transformation compared to normal pregnancy (Brosens et al, 1972).…”

Section: Preeclampsiamentioning

confidence: 99%