scholarly journals The interplay between thyroid hormones and the placenta: a comprehensive review†

2019 ◽  
Author(s):  
Enoch Appiah Adu-Gyamfi ◽  
Ying-Xiong Wang ◽  
Yu-Bin Ding
Keyword(s):  
Thyroid Hormones ◽  
Pregnancy Complications ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Molecular Mechanisms ◽  
Trophoblast Invasion ◽  
Trophoblast Differentiation ◽  
Comprehensive Review ◽  
Intrauterine Growth ◽  
The Relationship

Abstract Thyroid hormones (THs) regulate a number of metabolic processes during pregnancy. After implantation, the placenta forms and enhances embryonic growth and development. Dysregulated maternal THs signaling has been observed in malplacentation-mediated pregnancy complications such as preeclampsia, miscarriage, and intrauterine growth restriction (IUGR), but the molecular mechanisms involved in this association have not been fully characterized. In this review, we have discussed THs signaling and its roles in trophoblast proliferation, trophoblast differentiation, trophoblast invasion of the decidua, and decidual angiogenesis. We have also explored the relationship between specific pregnancy complications and placental THs transporters, deiodinases, and THs receptors. In addition, we have examined the effects of specific endocrine disruptors on placental THs signaling. The available evidence indicates that THs signaling is involved in the formation and functioning of the placenta and serves as the basis for understanding the pathogenesis and pathophysiology of dysthyroidism-associated pregnancy complications such as preeclampsia, miscarriage, and IUGR.

Antiphosphatidylserine/prothrombin Antibodies in Antiphospholipid Syndrome with Intrauterine Growth Restriction and Preeclampsia

2018 ◽  
Vol 45 (9) ◽  
pp. 1263-1272 ◽  
Author(s):  
Valentina Canti ◽  
Stefania Del Rosso ◽  
Marta Tonello ◽  
Roberta Lucianò ◽  
Ariela Hoxha ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Lupus Erythematosus ◽  
Pregnancy Complications ◽  
Intrauterine Growth Restriction ◽  
Late Pregnancy ◽  
Additional Treatment ◽  
Growth Restriction ◽  
Intrauterine Fetal Death ◽  
Thrombotic Risk ◽  
Intrauterine Growth

Objective.Antibodies that recognize the phosphatidylserine/prothrombin complex (antiphosphatidylserine/prothrombin antibodies; aPS/PT) might reveal enhanced thrombotic risk in patients with systemic lupus erythematosus. Little is known about their association with pregnancy complications in the antiphospholipid syndrome (APS).Methods.We enrolled 55 patients with APS who were seeking pregnancy in 2 Italian hospitals. Antiphospholipid antibodies (aPL), including anticardiolipin antibodies, anti-β2-glycoprotein I antibodies, lupus-like anticoagulant, and aPS/PT antibodies were assessed, and the patients were prospectively followed for 24 months.Results.There were 65% (36/55) of the APS patients who had aPS/PT antibodies. Forty-seven pregnancies were followed, including 33 of aPS/PT+ patients. Forty-one of the 47 patients (87%) who initiated a pregnancy eventually gave birth to a child. The pregnancy duration and the mean newborn weight at delivery were significantly lower in aPS/PT+ than in aPS/PT− patients (33.1 ± 4.7 vs 36.2 ± 3.4 wks of gestation, respectively, and 2058 ± 964 g vs 2784 ± 746 g, respectively, p < 0.05). Late pregnancy complications, including intrauterine fetal death, preterm delivery, preeclampsia, and intrauterine growth restriction (IUGR), were more frequent in aPS/PT+ patients, independent of the therapy. Titers of aPS/PT IgG were significantly inversely correlated with the neonatal weight at delivery. Vascular injury, as reflected by thrombosis, fibrinoid necrosis, ischemic and hemorrhagic areas, and presence of chorangiomas characterized the IUGR placentas in the presence of aPS/PT.Conclusion.The aPS/PT antibodies might represent markers of aPL-related pregnancy complications, IUGR/preeclampsia in particular, and could help identify beforehand patients who may require additional treatment.

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Ying-xue Ding ◽  
Hong Cui
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Growth Restriction ◽  
Microvascular Endothelial Cells ◽  
Intrauterine Growth ◽  
Growth Restrictions ◽  
The Brain

Abstract Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.

scholarly journals Perinatal Plasma Monocyte Chemotactic Protein-1 Concentrations in Intrauterine Growth Restriction

2007 ◽  
Vol 2007 ◽  
pp. 1-5 ◽  
Author(s):  
Despina D. Briana ◽  
Maria Boutsikou ◽  
Stavroula Baka ◽  
George Papadopoulos ◽  
Dimitrios Gourgiotis ◽  
...  
Keyword(s):  
Immune Response ◽  
Pregnancy Outcome ◽  
Gestational Age ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Trophoblast Invasion ◽  
Intrauterine Growth ◽  
Monocyte Chemotactic Protein ◽  
Chemotactic Protein ◽  
Appropriate For Gestational Age

Monocyte chemotactic protein-1 (MCP-1) plays vital roles in immune response, angiogenesis, and pregnancy outcome. We investigated plasma MCP-1 concentrations in 40 mothers and their 20 intrauterine-growth-restricted (IUGR) and 20 appropriate-for-gestational-age (AGA) fetuses and neonates on postnatal days 1 (N1) and 4 (N4). Maternal and fetal MCP-1 concentrations were decreased (P<001andP= .018, resp.), whereas N1 MCP-1 concentrations were elevated in IUGR group (P= .012). In both groups, fetal MCP-1 concentrations were lower compared to N1 and N4 ones (P= .045,P= .012, resp., for AGA,P<.001 in each case for IUGR). Reduced maternal and fetal MCP-1 concentrations in IUGR may reflect failure of trophoblast invasion, suggesting that down-regulation of MCP-1 may be involved in the pathogenesis of IUGR. Increased MCP-1 concentrations in IUGR neonates and higher postnatal ones in all infants may be attributed to gradual initiation of ex utero angiogenesis, which is possibly enhanced in IUGR.

The Relationship of Intrauterine Growth Restriction with Placental Pathologic Changes in Newborns

2020 ◽  
Author(s):  
Hossein Dalili ◽  
Fatemeh Sadat Nayeri ◽  
Seyed Reza Mirjalili ◽  
Seyyed Nasrollah Hossein ◽  
Alireza Abdollahi ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Pathological Examination ◽  
Histological Changes ◽  
Intrauterine Growth ◽  
Study Population ◽  
The Mean ◽  
Relationship Of ◽  
The Relationship ◽  
Restriction Group

Introduction: Intrauterine growth restriction is a multifaceted problem and is associated with a significant increase in the level of morbidity and perinatal mortality. According to some studies, failure of the placenta is responsible for the most cases of intrauterine growth restriction. The aim of this study was to evaluate the placental pathologic changes in the intrauterine growth restriction (IUGR) samples and compare them with normal cases.   Methods: A study population consisted of 60 intrauterine growth restriction neonates and 60 normalized neonates born at Tehran Imam Khomeini Hospital between June 2016 and July 2017. The placenta was weighed, immediately after delivery, and the umbilical cord was separated, then stored in 10% formalin and sent for pathological examination as soon as possible. Data collection was performed according to the following items: the pathologist's report, the results of the infants' examination, and the data in the neonatal cases.   Results: The intrauterine growth restriction group showed a high frequency of placenta infarction (P < 0.001), inflammation of the villous (P < 0.001), villous fibrosis (P = 0.044), villous vascularization disorder (P = 0.001), prevalence of chorioamnionitis (P = 0.027), prevalence of Syncytiotrophoblastic knots (P < 0.001) and placental necrosis (P = 0.048) than normal group. However, the mean weight of the placenta (P < 0.001), the length and width of the macroscopic placenta changes was less (P < 0.001).   Conclusion: The results of the current study showed that a major part of the macroscopic and histological changes are detectable in the intrauterine growth restriction samples, which are considerably more common than normal, although they are not pathognomonic, but in the future, more accurate results can be obtained from more extensive studies.

Placental HIF-1α, HIF-2α, membrane and soluble VEGF receptor-1 proteins are not increased in normotensive pregnancies complicated by late-onset intrauterine growth restriction

2007 ◽  
Vol 293 (2) ◽  
pp. R766-R774 ◽  
Author(s):  
Augustine Rajakumar ◽  
Arun Jeyabalan ◽  
Nina Markovic ◽  
Roberta Ness ◽  
Carol Gilmour ◽  
...  
Keyword(s):  
Northern Blot ◽  
Intrauterine Growth Restriction ◽  
Northern Blot Analysis ◽  
Late Onset ◽  
Growth Restriction ◽  
Trophoblast Invasion ◽  
Vegf Receptor ◽  
Placental Perfusion ◽  
Intrauterine Growth ◽  
Factor Α

Inadequate trophoblast invasion and spiral artery remodeling leading to poor placental perfusion are believed to underlie the pregnancy pathologies preeclampsia (PE) and intrauterine growth restriction (IUGR). The main objective of this study was to investigate hypoxia-inducible transcription factor-α (HIF-α) and downstream genes (VEGF receptor-1) Flt-1 and soluble fms-like tyrosine kinase 1 (sFlt-1) proteins in IUGR placentas. Placentas from normal pregnant (NP; n = 18), PE ( n = 18), and IUGR ( n = 10) patients were investigated. Normotensive patients with IUGR delivered babies at ≥ 37 wk of gestation with birth weights of <10% and asymmetrical growth. HIF-1α, -2α, Flt-1, and sFlt-1 protein, and mRNA were assessed by Western and Northern blot analyses, respectively. The results are expressed as ratios of the densitometric values for each pair of pathologic and normal placentas, a ratio of 1.0 indicating no difference. Comparable to our earlier studies, the PE/NP ratios for HIF-1α, -2α, and Flt proteins were significantly increased by 50–100% (all P < 0.01 vs. 1.0). Unexpectedly, the IUGR/NP ratios for HIF-1α and -2α proteins were 1.03 ± 0.07 and 0.96 ± 0.16, respectively, and for Flt and sFlt were 1.14 ± 0.15 and 0.95 ± 0.12, respectively (all P = not significant vs. 1.0). Northern blot analysis revealed comparable levels of HIF-α mRNA in abnormal and normal placentas. In contrast to PE, HIF-α proteins and regulated genes are not increased in placentas from normotensive pregnant women delivering small, asymmetrically grown babies ≥ 37 wk of gestation. The absence of an increase in HIF-α protein is not due to insufficient HIF-α mRNA for protein synthesis. Thus, the placentas from women with PE and late IUGR are fundamentally different at the molecular level.

scholarly journals Selenium is a functional component of the female reproductive system. Its role in pregnancy complications

2021 ◽  
Vol 4 (4) ◽  
pp. 328-332
Author(s):  
G.K. Sadykova ◽  
◽  
A.A. Olina ◽  
◽  
Keyword(s):  
Reproductive System ◽  
Pregnancy Complications ◽  
Premature Birth ◽  
Intrauterine Growth Restriction ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Female Reproductive System ◽  
Functional Component ◽  
Intrauterine Growth ◽  
In Pregnancy

This paper reviews studies on selenium (Se) in human reproduction. Low Se intake is associated with the development of gestational hypertension, miscarriage, premature birth, intrauterine growth restriction, and thyroid gland dysfunction. Therefore, studies on the association between Se deficiency and impaired folliculogenesis, steroidogenesis, and infertility in women are of great interest. Unfortunately, these studies are scarce, and further studies are needed. A significant antioxidant activity of Se-containing enzymes allows for minimizing risks of obstetrical complications associated with placental insufficiency. Therefore, selenium is vital for realizing female reproductive function. However, even given potential risks of insufficient Se-containing product intake, the authors find it unacceptable to recommend Se dotation in the population since toxic effects of Se excess are yet to be fully explored. Further studies on Se biological effects will extend the scope of its use in obstetrics and gynecology in terms of a preventive approach. KEYWORDS: selenium, placental insufficiency, folliculogenesis, steroidogenesis, antioxidant, miscarriage, premature birth, intrauterine growth restriction. FOR CITATION: Sadykova G.K., Olina A.A. Selenium is a functional component of the female reproductive system. Its role in pregnancy complications. Russian Journal of Woman and Child Health. 2021;4(4):328–332 (in Russ.). DOI: 10.32364/2618-8430-2021-4-4- 328-332.

The relationship between cadmium and lead with selenium, copper and zinc in normal and intrauterine growth restriction pregnancy

2007 ◽  
Vol 172 ◽  
pp. S178-S179
Author(s):  
Suzana Cavar ◽  
Tomislav Klapec ◽  
Zoran Kasac ◽  
Silvija Rucevic ◽  
Ana Popinjac ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Copper And Zinc ◽  
Cadmium And Lead ◽  
The Relationship

scholarly journals Human Cytomegalovirus Infection Interferes with the Maintenance and Differentiation of Trophoblast Progenitor Cells of the Human Placenta

2015 ◽  
Vol 89 (9) ◽  
pp. 5134-5147 ◽  
Author(s):  
Takako Tabata ◽  
Matthew Petitt ◽  
Martin Zydek ◽  
June Fang-Hoover ◽  
Nicholas Larocque ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Human Cytomegalovirus ◽  
Intrauterine Growth Restriction ◽  
Molecular Mechanisms ◽  
Hcmv Infection ◽  
Congenital Infection ◽  
Growth Restriction ◽  
Chorionic Villi ◽  
Intrauterine Growth

ABSTRACTHuman cytomegalovirus (HCMV) is a major cause of birth defects that include severe neurological deficits, hearing and vision loss, and intrauterine growth restriction. Viral infection of the placenta leads to development of avascular villi, edema, and hypoxia associated with symptomatic congenital infection. Studies of primary cytotrophoblasts (CTBs) revealed that HCMV infection impedes terminal stages of differentiation and invasion by various molecular mechanisms. We recently discovered that HCMV arrests earlier stages involving development of human trophoblast progenitor cells (TBPCs), which give rise to the mature cell types of chorionic villi—syncytiotrophoblasts on the surfaces of floating villi and invasive CTBs that remodel the uterine vasculature. Here, we show that viral proteins are present in TBPCs of the chorion in cases of symptomatic congenital infection.In vitrostudies revealed that HCMV replicates in continuously self-renewing TBPC lines derived from the chorion and alters expression and subcellular localization of proteins required for cell cycle progression, pluripotency, and early differentiation. In addition, treatment with a human monoclonal antibody to HCMV glycoprotein B rescues differentiation capacity, and thus, TBPCs have potential utility for evaluation of the efficacies of novel antiviral antibodies in protecting and restoring placental development. Our results suggest that HCMV replicates in TBPCs in the chorionin vivo, interfering with the earliest steps in the growth of new villi, contributing to virus transmission and impairing compensatory development. In cases of congenital infection, reduced responsiveness of the placenta to hypoxia limits the transport of substances from maternal blood and contributes to fetal growth restriction.IMPORTANCEHuman cytomegalovirus (HCMV) is a leading cause of birth defects in the United States. Congenital infection can result in permanent neurological defects, mental retardation, hearing loss, visual impairment, and pregnancy complications, including intrauterine growth restriction, preterm delivery, and stillbirth. Currently, there is neither a vaccine nor any approved treatment for congenital HCMV infection during gestation. The molecular mechanisms underlying structural deficiencies in the placenta that undermine fetal development are poorly understood. Here we report that HCMV replicates in trophoblast progenitor cells (TBPCs)—precursors of the mature placental cells, syncytiotrophoblasts and cytotrophoblasts, in chorionic villi—in clinical cases of congenital infection. Virus replication in TBPCsin vitrodysregulates key proteins required for self-renewal and differentiation and inhibits normal division and development into mature placental cells. Our findings provide insights into the underlying molecular mechanisms by which HCMV replication interferes with placental maturation and transport functions.

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