Placental Growth from the First to the Second Trimester of Pregnancy in SGA-foetuses and Pre-eclamptic Pregnancies Compared to Normal Foetuses

Hafner, E.; Metzenbauer, M.; Höfinger, D.; Münkel, Meret; Gassner, Rainer; Schuchter, K.; Dillinger-Paller, B.; Philipp, K

doi:10.1053/plac.2002.0918

Cited by 110 publications

(80 citation statements)

References 7 publications

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“…Thus in cases of intrauterine growth restriction the placenta is smaller than normal at 12 weeks but grows at the same rate thereafter. If there is accompanying preeclampsia, however, the subsequent rate of growth is slowed (Hafner et al, 2003). In cases of lateonset preeclampsia placental size is often increased at 12 weeks, but then the rate of growth slows between 16 and 20 weeks.…”

Section: B Amentioning

confidence: 99%

The influence of the intrauterine environment on human placental development

Jauniaux²,

2010

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Development of the human placenta is modulated heavily by the intrauterine environment. During the first trimester, development takes place in a low oxygen environment supported by histiotrophic nutrition from the endometrial glands. Consequently, the rate of growth of the chorionic sac is almost invariable across this period, and is remarkably uniform between individuals. Towards the end of the first trimester the intrauterine environment undergoes radical transformation in association with onset of the maternal arterial circulation and the switch to haemotrophic nutrition. The accompanying rise in intraplacental oxygen concentration poses a major challenge to placental tissues, and extensive villous remodelling takes place at this time. Later in pregnancy a wide variety of stressors are capable of affecting placental growth, but in the human, the most common are nutrient deprivation and vascular compromise. The latter is usually secondary to deficient trophoblast invasion and can induce placental oxidative stress. Closely linked to oxidative stress is endoplasmic reticulum stress, and we recently provided the first evidence that the latter plays a major role in the pathophysiology of intrauterine growth restriction. The endoplasmic reticulum is a key regulator of protein synthesis, exerting its effects through the unfolded protein response. Consequently, we observed multiple blocks to translation initiation and elongation in growth restricted placentas. Nutrient deprivation also modulates protein synthesis through the mTOR pathway, and we demonstrated interactions between this pathway and endoplasmic reticulum stress. Protein synthesis inhibition therefore appears to be a common mechanism for regulating placental development under different adverse conditions.

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Section: B Amentioning

confidence: 99%

The influence of the intrauterine environment on human placental development

Jauniaux²,

2010

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“…Thus, during human pregnancy, reduced placental growth precedes fetal IUGR. 2,3 There are many potential causes of human IUGR, including maternal smoking, undernutrition, infection, or congenital malformations, but the majority of cases remain unexplained. Nonetheless, these are frequently associated with deficient conversion of the maternal spiral arteries supplying the placenta.…”

mentioning

confidence: 99%

Evidence of Placental Translation Inhibition and Endoplasmic Reticulum Stress in the Etiology of Human Intrauterine Growth Restriction

Yung

Calabrese

Hynx

et al. 2008

The American Journal of Pathology

335

304

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Unexplained intrauterine growth restriction of the fetus (IUGR) results from impaired placental development, frequently associated with maternal malperfusion. Some cases are complicated further by preeclampsia (PE؉IUGR). Here, we provide the first evidence that placental protein synthesis inhibition and endoplasmic reticulum (ER) stress play key roles in IUGR pathophysiology. Increased phosphorylation of eukaryotic initiation factor 2␣ suggests suppression of translation initiation in IUGR placentas, with a further increase in PE؉IUGR cases. Consequently, AKT levels were reduced at the protein, but not mRNA, level. Additionally, levels of other proteins in the AKT-mammalian target of rapamycin pathway were decreased, and there was associated dephosphorylation of 4E-binding protein 1 and activation of glycogen synthase kinase 3␤. Cyclin D1 and the eukaryotic initiation factor 2B epsilon subunit were also down-regulated, providing additional evidence for this placental phenotype. The central role of AKT signaling in placental growth regulation was confirmed in Akt1 null mice, which display IUGR. In addition, we demonstrated ultrastructural and molecular evidence of ER stress in human IUGR and PE؉IUGR placentas, providing a potential mechanism for eukaryotic initiation factor 2␣ phosphorylation. In confirmation, induction of low-grade ER stress in trophoblast-like cell lines reduced cellular proliferation. PE؉IUGR placentas showed elevated ER stress with the additional expression of the pro-apoptotic protein C/EBP-homologous protein/growth arrest and DNA damage 153. These findings may account for the increased microparticulate placental debris in the maternal circulation of these cases, leading to endothelial cell activation and impairing placental development.

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“…However, the number of polymorphisms does not seem to influence the risk for concurrent development of HELLP syndrome or IUGR in women with pre-eclampsia. Instead the occurrence of these additional complications may relate to the time of onset of the placental pathology during pregnancy [22] .…”

Section: Discussionmentioning

confidence: 99%

Susceptibility to Pre-Eclampsia Is Associated with Multiple Genetic Polymorphisms in Maternal Biotransformation Enzymes

Zusterzeel¹,

Peters²,

Burton

et al. 2006

Gynecol Obstet Invest

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Background/Aims: Probably no single gene is responsible for pre-eclampsia, but the disease merely is the result of polymorphisms in several genes in association with environmental factors. We therefore studied the simultaneous occurrence of several genetic polymorphisms in biotransformation enzymes in women who had developed pre- eclampsia, either with or without the HELLP syndrome, in comparison with healthy controls. Methods: The results of two previous studies on genetic polymorphisms in glutathione S-transferases P1, M1 and T1, epoxide hydrolase (EPHX) and cytochrome P4501A1 (CYP1A1) in 167 women with a history of pre-eclampsia and in 110 controls were combined. χ² analyses were used for statistical evaluation of the number of polymorphisms between cases and controls. Results: There was a significant association with the number of genetic polymorphisms in biotransformation enzymes, pointing at an increased toxification or decreased detoxification, in women with a history of pre-eclampsia, as compared to healthy controls (p < 0.001). Conclusion: Women withthe simultaneous occurrence of two or more genetic polymorphisms in the above-mentioned biotransformation enzymes, most probably resulting in a disturbed detoxification capacity, may be at increased risk for pre-eclampsia.

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Placental Growth from the First to the Second Trimester of Pregnancy in SGA-foetuses and Pre-eclamptic Pregnancies Compared to Normal Foetuses

Cited by 110 publications

References 7 publications

The influence of the intrauterine environment on human placental development

The influence of the intrauterine environment on human placental development

Evidence of Placental Translation Inhibition and Endoplasmic Reticulum Stress in the Etiology of Human Intrauterine Growth Restriction

Susceptibility to Pre-Eclampsia Is Associated with Multiple Genetic Polymorphisms in Maternal Biotransformation Enzymes

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