Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

Wageh, Alaa; Nagib, Reham M; Eid, Mohamed I

doi:10.21608/ebwhj.2019.33481

Cited by 3 publications

(3 citation statements)

References 26 publications

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“…This may be attributed to histoimmunologic changes in the placenta of late-onset PE fetuses, albeit less severe than with earlyonset PE. 27 With a high predictive value for CVD, carotid-femoral PWV is considered to be a gold standard to measure arterial stiffness. 18 Despite its predictive ability and ease of measurement, there is limited literature on PWV changes in children exposed to PE.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Dysfunction in Children Exposed to Preeclampsia During Fetal Life

Hoodbhoy

Mohammed

Rozi

et al. 2021

Journal of the American Society of Echocardiography

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Background: Keeping in view the developmental origin of health and disease hypothesis, the aim of this study was to assess differences in cardiac and vascular structure and function in children exposed to preeclampsia in utero compared with those of normotensive mothers. The hypothesis under investigation was that children exposed to preeclampsia would have altered cardiac and vascular structure and function compared with the unexposed group.Methods: This was a retrospective cohort study that included children 2 to 10 years of age born to mothers with and without exposure to preeclampsia in utero (n = 80 in each group). Myocardial morphology and function using echocardiography and carotid intima-media thickness and pulse-wave velocity were determined. Multivariate linear regression was used to compare preeclampsia-exposed and nonexposed groups. Subgroup analysis to assess differences between early-and late-onset preeclampsia was also performed.Results: Forty-one percent of mothers (n = 33) had early-onset preeclampsia. Children in the exposed group had a significantly higher prevalence of stage 1 systolic and diastolic hypertension (22% [n = 18] and 35% [n = 18], respectively) compared with the unexposed group (9% [n = 7] and 19% [n = 15], respectively; P = .01). Children in the exposed group also had higher pulse-wave velocity compared with those in the unexposed group (0.42 6 0.1 vs 0.39 6 0.1, P = .03). Subgroup analysis revealed that changes in blood pressure and pulse-wave velocity were determined primarily by early-onset preeclampsia. There was no significant difference in cardiac morphology or systolic and diastolic function between the exposed and unexposed groups. Conclusion:In utero exposure to preeclampsia has an effect on vascular function in children aged 2 to 10 years, related primarily to early-onset disease. Routine blood pressure screening should be recommended for such children.

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Section: Discussionmentioning

confidence: 99%

Cardiovascular Dysfunction in Children Exposed to Preeclampsia During Fetal Life

Hoodbhoy

Mohammed

Rozi

et al. 2021

Journal of the American Society of Echocardiography

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“…The significance of Smad3 inactivation in late onset PE is not clear; however, the TGF-β family has been reported to regulate other aspects of placenta functions, such as apoptosis (25,29). Dysregulation of villous trophoblast apoptosis is also observed in late onset PE (67). The role of Smad3 in this process remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Differential Role of Smad2 and Smad3 in the Acquisition of an Endovascular Trophoblast-Like Phenotype and Preeclampsia

et al. 2020

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During placental development, cytotrophoblast progenitor cells differentiate into the syncytiotrophoblast and invasive extravillous trophoblasts (EVTs). Some EVTs further differentiate into endovascular trophoblasts (enEVTs) which exhibit endothelial-like properties. Abnormal placental development, including insufficient enEVT-mediated remodeling of the uterine spiral arteries, is thought to be a precipitating factor in the onset of preeclampsia (PE), a pregnancy-related hypertensive disorder. Several members of the transforming growth factor-β (TGF-β) superfamily, such as TGF-βs, Nodal, and Activin have been reported to either promote or inhibit the invasive EVT pathway. These ligands signal through serine/threonine receptor complexes to activate downstream signaling mediators, Smad2 and Smad3. In this study, we determined Smad2 and Smad3 expression pattern in placenta and their effects on trophoblast invasion and differentiation. Total Smad2/3 levels were relatively constant across gestation while the ratio of active phosphorylated forms to their total levels varied with gestational stages, with a higher pSmad2/total Smad2 in later gestation and a higher pSmad3/total Smad3 in early gestation. Immunofluorescent staining revealed that pSmad3 was localized in nuclei of EVTs in anchoring villi. On the other hand, pSmad2 was mostly absent in this invasive EVT population. In addition, pSmad3/total Smad3, but not pSmad2/total Smad2, was significantly lower in both early onset and late onset PE cases, as compared to gestational age-matched controls. Functional studies carried out using a first trimester trophoblast cell line, HTR-8/SVneo, and first trimester human placental explants showed that Smad2 and Smad3 had differential roles in the invasive pathway. Specifically, siRNA-mediated knockdown of Smad2 resulted in an increase in trophoblast invasion and an upregulation of mRNA levels of enEVT markers while the opposite was observed with Smad3 knockdown. In addition, Smad2 siRNA accelerated the EVT outgrowth in first trimester placental explants while the Smad3 siRNA reduced the outgrowth of EVTs when compared to the control. Furthermore, knockdown of Smad2 enhanced, whereas overexpression of Smad2 suppressed, the ability of trophoblasts to form Brkić et al. Differential Role of Smad2 and Smad3 in Placenta endothelial-like networks. Conversely, Smad3 had opposite effects as Smad2 on network formation. These findings suggest that Smad2 and Smad3 have opposite functions in the acquisition of an enEVT-like phenotype and defects in Smad3 activation are associated with PE.

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“…A considerable body of evidence indicates that blood from patients with preeclampsia demonstrates a high level of inflammatory factors (such as: TNF-α, IFN-γ, IL6 or IL1) and reactive oxygen species (ROS), and that preeclamptic placentas display features indicative of chronic hypoxia throughout the gestation period [ 5 , 6 , 7 ]. Inflammation, oxidative stress, ineffective angiogenesis, and hypoxia are regulated at the cellular level by numerous pathways, most of which are under the control of nuclear factor kappa B (NFĸB) [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

The Targeting of Nuclear Factor Kappa B by Drugs Adopted for the Prevention and Treatment of Preeclampsia

Sakowicz

2022

IJMS

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Preeclampsia (PE) is characterised by high levels and activity of the transcription factor Nuclear Factor kappa B (NFĸB) in the maternal blood and placental cells. This factor is responsible for the regulation of over 400 genes known to influence processes related to inflammation, apoptosis and angiogenesis, and cellular responses to oxidative stress and hypoxia. Although high NFĸB activity induces hypoxia and inflammation, which are beneficial for the process of implantation, NFĸB level should be reduced in the later stages of physiological pregnancy to favour maternal immunosuppression and maintain gestation. It is believed that the downregulation of NFĸB activity by pharmacotherapy might be a promising way to treat preeclampsia. Interestingly, many of the drugs adopted for the prevention and treatment of preeclampsia have been found to regulate NFĸB activity. Despite this, further innovation is urgently needed to ensure treatment safety and efficacy. The present article summarizes the current state of knowledge about the drugs recommended by cardiology, obstetrics, and gynaecology societies for the prevention and treatment of preeclampsia with regard to their impact on the cellular regulation of NFĸB pathways.

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Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

Cited by 3 publications

References 26 publications

Cardiovascular Dysfunction in Children Exposed to Preeclampsia During Fetal Life

Cardiovascular Dysfunction in Children Exposed to Preeclampsia During Fetal Life

Differential Role of Smad2 and Smad3 in the Acquisition of an Endovascular Trophoblast-Like Phenotype and Preeclampsia

The Targeting of Nuclear Factor Kappa B by Drugs Adopted for the Prevention and Treatment of Preeclampsia

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