The placenta

2020 ◽  
pp. 120-132
Author(s):  
Eric Jauniaux ◽  
Amarnath Bhide ◽  
Graham J. Burton
Keyword(s):  
Steroid Hormones ◽  
Fetal Growth ◽  
Placenta Praevia ◽  
Direct Impact ◽  
Perinatal Complications ◽  
Placental Development ◽  
Vast Array ◽  
Antenatal Detection ◽  
And Function ◽  
In Pregnancy

Abnormal placental development and function are widely recognized as having immediate consequences on the outcome of a pregnancy, and more recently to influence the lifelong health of the offspring. The development of the placenta starts from implantation, when the embryonic pole of the blastocyst enters into contact with the maternal uterine epithelium. The placenta provides the fetus with all essential nutrients, water, and oxygen, and a route for clearance of fetal excretory products, but it also produces a vast array of protein and steroid hormones and factors necessary for the maintenance of pregnancy. Placental-related disorders of pregnancy affect around a third of human pregnancies, primarily including miscarriages, pre-eclampsia, and fetal growth restriction. Placental and umbilical cord structural anomalies that are associated with perinatal complications can now be diagnosed from early in pregnancy with ultrasonography and the antenatal detection of anomalies such as placenta praevia and placenta accreta has a direct impact on the outcome of pregnancy.

Adaptability and potential for treatment of placental functions to improve embryonic development and postnatal health

2016 ◽  
Vol 28 (2) ◽  
pp. 75 ◽  
Author(s):  
James C. Cross
Keyword(s):  
Fetal Growth ◽  
Growth And Development ◽  
Association Studies ◽  
Experimental Studies ◽  
Placental Development ◽  
Experimental Animals ◽  
And Function ◽  
The Impact ◽  
Lines Of Evidence ◽  
In Pregnancy

For an organ that is so critical for life in eutherian mammals, the placenta hardly gets the attention that it deserves. The placenta does a series of remarkable things, including implanting the embryo in the uterus, negotiating with the mother for nutrients but also protecting her health during pregnancy, helping establish normal metabolic and cardiovascular function for life postnatally (developmental programming) and initiating changes that prepare the mother to care for and suckle her young after birth. Different lines of evidence in experimental animals suggest that the development and function of the placenta are adaptable. This means that some of the changes observed in pathological pregnancies may represent attempts to mitigate the impact of fetal growth and development. Key and emerging concepts are reviewed here concerning how we may view the placenta diagnostically and therapeutically in pregnancy complications, focusing on information from experimental studies in mice, sheep and cattle, as well as association studies from humans. Hundreds of different genes have been shown to underlie normal placental development and function, some of which have promise as tractable targets for intervention in pregnancies at risk for poor fetal growth.

Placental control of fetal growth

1995 ◽  
Vol 7 (3) ◽  
pp. 333 ◽  
Author(s):  
J Robinson ◽  
S Chidzanja ◽  
K Kind ◽  
F Lok ◽  
P Owens ◽  
...  
Keyword(s):  
Growth Factors ◽  
Fetal Growth ◽  
Placental Development ◽  
Maternal Environment ◽  
Adult Disease ◽  
Prenatal Growth ◽  
And Function ◽  
Subsequent Risk ◽  
Length Of Gestation ◽  
Insulin Like Growth Factors

The placenta exerts its effects on the growth of the fetus from the beginning of pregnancy via metabolic and endocrine mechanisms. To achieve this, the placenta exchanges a wide array of nutrients, endocrine signals, cytokines and growth factors with the mother and the fetus. These exchanges modulate or programme fetal growth and development. This review concentrates on the function and structure of the placenta in humans and in animals, and the effects of experimental perturbation of placental size and function on fetal growth. The consequences for fetal growth of varying the abundance of peptides or, by deleting genes, insulin-like growth factors or cytokines, are also described. Maternal nutritional and hormonal state from as early as the first few days after fertilization, can influence the growth rate of the placenta and the fetus and also the length of gestation. Influences on placental development and their consequences will clearly have an impact on the placental control of fetal growth. Variations in the maternal environment and consequent perturbation of the metabolic and endocrine environment of the placenta and fetus are implicated as being responsible for the associations between prenatal growth of the placenta and its fetus and the subsequent risk of adult disease. The next challenge will be to determine the dominant influences at each stage of fetal and placental growth.

Maternal Methyl-Cycle Amino Acid Profile and Kinetics: Relation with Placental Growth

2017 ◽  
Vol 54 (2) ◽  
pp. 118
Author(s):  
Sarita Devi ◽  
Julian Crasta ◽  
Tinku Thomas ◽  
Pratibha Dwarkanath ◽  
Annamma Thomas ◽  
...  
Keyword(s):  
Amino Acid ◽  
Pregnant Women ◽  
Fetal Growth ◽  
Secondary Analysis ◽  
Placental Development ◽  
Amino Acid Availability ◽  
South Indian ◽  
Methyl Cycle ◽  
And Function ◽  
Amino Acid Concentrations

Maternal intake of quality protein regulates placental development and function thereby affecting fetal growth. Considering the prevalence of inadequate intakes of quality protein in Indian pregnant women, understanding the interplay between maternal supply of protein, its metabolism and fetoplacental growth becomes important. A secondary analysis of data from an open labelled-randomized intervention trial with 500 ml milk/day on south Indian pregnant women with marginally low vitamin B12 status, was performed to assess the relations between placental parameters and maternal trimester 3 methyl-cycle amino acid status as well as kinetics. This analysis was performed for 42 pregnancies from the trial where placentae had been collected and placental parameters had been measured. For these pregnancies, data on trimester 3 methionine, serine and glycine kinetics as well as plasma free amino acid concentrations were available. Protein intake and plasma citrulline concentrations were positively correlated at trimester 3 (ρ = 0.34, P = 0.027). Placental weight correlated positively with methyl-cycle specific amino acid concentrations [methionine (ρ = 0.32, P = 0.0388), serine (ρ = 0.49, P = 0.0009)], methionine kinetics [total methionine flux rates (ρ = 0.42, P = 0.006), RM (ρ = 0.45, P = 0.003), TS (ρ = 0.32, P = 0.046), TM (ρ = 0.45, P = 0.004)] and with birth weight (ρ = 0.57, P < 0.001). Findings from the current study indicate that maternal amino acid availability and more importantly, maternal methionine kinetics, positively influenced placental growth, likely mediated by key amino acids such as citrulline, which is known to regulate placental blood flow and function. As an appropriately functioning placenta is indispensable for fetal growth, these findings will form the basis for detailed mechanistic explorations into the placental regulation of maternal supply of amino acid to the fetus for designing effective intervention strategies towards optimizing fetomaternal health during and after pregnancy.

scholarly journals Maternal growth factor regulation of human placental development and fetal growth

2010 ◽  
Vol 207 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Karen Forbes ◽  
Melissa Westwood
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Fetal Growth ◽  
Mechanism Of Action ◽  
Normal Development ◽  
Receptor Interaction ◽  
Placental Development ◽  
Maternal Circulation ◽  
Successful Pregnancy ◽  
And Function

Normal development and function of the placenta is critical to achieving a successful pregnancy, as normal fetal growth depends directly on the transfer of nutrients from mother to fetus via this organ. Recently, it has become apparent from both animal and human studies that growth factors within the maternal circulation, for example the IGFs, are important regulators of placental development and function. Although these factors act via distinct receptors to exert their effects, the downstream molecules activated upon ligand/receptor interaction are common to many growth factors. The expression of numerous signaling molecules is altered in the placentas from pregnancies affected by the fetal growth complications, fetal growth restriction, and macrosomia. Thus, targeting these molecules may lead to more effective treatments for complications of pregnancy associated with altered placental development. Here, we review the maternal growth factors required for placental development and discuss their mechanism of action.

scholarly journals Abnormalities of placental development and function are associated with the different fetal growth patterns of hypoplastic left heart syndrome and transposition of the great arteries

2018 ◽  
Author(s):  
Weston Troja ◽  
Kathryn J. Owens ◽  
Jennifer Courtney ◽  
Andrea C. Hinton ◽  
Robert B. Hinton ◽  
...  
Keyword(s):  
Hypoplastic Left Heart Syndrome ◽  
Fetal Growth ◽  
Weight Ratio ◽  
Growth Patterns ◽  
Left Heart ◽  
Placental Development ◽  
Hypoplastic Left Heart ◽  
Terminal Villi ◽  
And Function ◽  
Left Heart Syndrome

AbstractBackgroundBirthweight is a critical predictor of congenital heart disease (CHD) surgical outcomes. Hypoplastic left heart syndrome (HLHS) is cyanotic CHD with known fetal growth restriction and placental abnormalities. Transposition of the great arteries (TGA) is cyanotic CHD with normal fetal growth. Comparison of the placenta in these diagnoses may provide insights on the fetal growth abnormality of CHD.MethodsClinical data and placental histology from placentas associated with Transposition of the Great Arteries (TGA) were analyzed for gross pathology, morphology, maturity and vascularity and compared to both control and previously analyzed HLHS placentas [1]. RNA was isolated from HLHS, TGA and control placentas and sequenced by Illumina HiSeq.Gene, analysis was performed using TopHat, R and MSigDB. Cluster analysis was performed using GoElite and Pathway analysis performed using PANTHERdb Overrepresentation Test. Immunohistochemistry was utilized to assess placental nutrient transporter expression in all three groups.ResultsPlacental weight was reduced in TGA cases, and demonstrated reduced villous vasculature, immature terminal villi, and increased fibrin deposition in the parenchyma compared to controls and reflected our previous data from HLHS placentas. However, birth weight was not reduced in TGA cases compared to controls in contrast to the HLHS cohort and birthweight:placental weight ratio was significantly increased in TGA cases but not HLHS compared to control. Need to include RNA and IHC.ConclusionsDespite common vascular disturbances in placentas from HLHAs and TGA, these do not account for the

scholarly journals The potential role of the ERRγ pathway in placental dysfunction

Reproduction ◽  
2020 ◽  
Author(s):  
Zhiyong Zou ◽  
Karen Forbes ◽  
Lynda K. Harris ◽  
Alexander E P Heazell
Keyword(s):  
Fetal Growth ◽  
Therapeutic Interventions ◽  
Placental Development ◽  
Human Trophoblast ◽  
Altered Expression ◽  
Placental Dysfunction ◽  
And Function ◽  
Upstream Regulators ◽  
Estrogen Related Receptor

Normal placental development and function is of key importance to fetal growth. Conversely aberrations of placental structure and function are evident in pregnancy complications including fetal growth restriction (FGR) and preeclampsia. Although trophoblast turnover and function is altered in these conditions, their underlying aetiologies and pathophysiology remains unclear, which hampers development of therapeutic interventions. Here we review evidence that supports a role for Estrogen Related Receptor-gamma (ERRγ) in the development of placental dysfunction in FGR and preeclampsia. This relationship deserves particular consideration because ERRγ is highly expressed in normal placenta, is reduced in FGR and preeclampsia and its expression is altered by hypoxia, which is thought to result from deficient placentation seen in FGR and preeclampsia. Several studies have also found microRNA or other potential upstream regulators of ERRγ negatively influence trophoblast function which could contribute to placental dysfunction seen in FGR and preeclampsia. Interestingly, microRNAs regulate ERRγ expression in human trophoblast. Thus, if ERRγ is pivotally associated with the abnormal trophoblast turnover and function it may be targeted by microRNAs or other possible upstream regulators in the placenta. This review explores altered expression of ERRγ and upstream regulation of ERRγ-mediated pathways resulting in the trophoblast turnover, placental vascularisation, and placental metabolism underlying placental dysfunctions. This demonstrates that the ERRγ pathway merits further investigation as a potential therapeutic target in FGR and preeclampsia.

scholarly journals Malaria in Pregnancy: From Placental Infection to Its Abnormal Development and Damage

2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Lin Lin Chua ◽  
Sebastian Kah Ming Khoo ◽  
Jun Long Ernest Ong ◽  
Gaurav Kumar Ramireddi ◽  
Tsin Wen Yeo ◽  
...  
Keyword(s):  
Placental Malaria ◽  
Parasitic Infection ◽  
Malaria In Pregnancy ◽  
Abnormal Development ◽  
Placental Development ◽  
Mortality And Morbidity ◽  
Effective Interventions ◽  
Histopathological Studies ◽  
And Function ◽  
In Pregnancy

Malaria remains a global health burden with Plasmodium falciparum accounting for the highest mortality and morbidity. Malaria in pregnancy can lead to the development of placental malaria, where P. falciparum-infected erythrocytes adhere to placental receptors, triggering placental inflammation and subsequent damage, causing harm to both mother and her infant. Histopathological studies of P. falciparum-infected placentas revealed various placental abnormalities such as excessive perivillous fibrinoid deposits, breakdown of syncytiotrophoblast integrity, trophoblast basal lamina thickening, increased syncytial knotting, and accumulation of mononuclear immune cells within intervillous spaces. These events in turn, are likely to impair placental development and function, ultimately causing placental insufficiency, intrauterine growth restriction, preterm delivery and low birth weight. Hence, a better understanding of the mechanisms behind placental alterations and damage during placental malaria is needed for the design of effective interventions. In this review, using evidence from human studies and murine models, an integrated view on the potential mechanisms underlying placental pathologies in malaria in pregnancy is provided. The molecular, immunological and metabolic changes in infected placentas that reflect their responses to the parasitic infection and injury are discussed. Finally, potential models that can be used by researchers to improve our understanding on the pathogenesis of malaria in pregnancy and placental pathologies are presented.

scholarly journals Circulating IGF1 and IGF2 and SNP genotypes in men and pregnant and non-pregnant women

2014 ◽  
Vol 3 (3) ◽  
pp. 138-149 ◽  
Author(s):  
K L Gatford ◽  
G K Heinemann ◽  
S D Thompson ◽  
J V Zhang ◽  
S Buckberry ◽  
...  
Keyword(s):  
Linkage Disequilibrium ◽  
Pregnant Women ◽  
Postnatal Growth ◽  
Candidate Snps ◽  
Nucleotide Polymorphisms ◽  
Placental Development ◽  
Single Nucleotide ◽  
Adults And Children ◽  
And Function ◽  
In Pregnancy

Circulating IGFs are important regulators of prenatal and postnatal growth, and of metabolism and pregnancy, and change with sex, age and pregnancy. Single-nucleotide polymorphisms (SNPs) in genes coding for these hormones associate with circulating abundance of IGF1 and IGF2 in non-pregnant adults and children, but whether this occurs in pregnancy is unknown. We therefore investigated associations of plasma IGF1 and IGF2 with age and genotype at candidate SNPs previously associated with circulating IGF1, IGF2 or methylation of the INS–IGF2–H19 locus in men (n=134), non-pregnant women (n=74) and women at 15 weeks of gestation (n=98). Plasma IGF1 concentrations decreased with age (P<0.001) and plasma IGF1 and IGF2 concentrations were lower in pregnant women than in non-pregnant women or men (each P<0.001). SNP genotypes in the INS–IGF2–H19 locus were associated with plasma IGF1 (IGF2 rs680, IGF2 rs1004446 and IGF2 rs3741204) and IGF2 (IGF2 rs1004446, IGF2 rs3741204 and H19 rs217727). In single SNP models, effects of IGF2 rs680 were similar between groups, with higher plasma IGF1 concentrations in individuals with the GG genotype when compared with GA (P=0.016), or combined GA and AA genotypes (P=0.003). SNPs in the IGF2 gene associated with IGF1 or IGF2 were in linkage disequilibrium, hence these associations could reflect other genotype variations within this region or be due to changes in INS–IGF2–H19 methylation previously associated with some of these variants. As IGF1 in early pregnancy promotes placental differentiation and function, lower IGF1 concentrations in pregnant women carrying IGF2 rs680 A alleles may affect placental development and/or risk of pregnancy complications.

scholarly journals A role for maternally derived myokines to optimize placental function and fetal growth across gestation

2017 ◽  
Vol 42 (5) ◽  
pp. 459-469 ◽  
Author(s):  
Chantal Dubé ◽  
Céline Aguer ◽  
Kristi Adamo ◽  
Shannon Bainbridge
Keyword(s):  
Protective Effect ◽  
Fetal Growth ◽  
Skeletal Muscles ◽  
Strong Support ◽  
Therapeutic Interventions ◽  
Placental Development ◽  
Maternal Exercise ◽  
Exercise Induced ◽  
And Function ◽  
Exercise During Pregnancy

Exercise during pregnancy is associated with improved health outcomes for both mother and baby, including a reduced risk of future obesity and susceptibility to chronic diseases. Overwhelming evidence demonstrates a protective effect of maternal exercise against fetal birth weight extremes, reducing the rates of both large- and small-for-gestational-age infants. It is speculated that this protective effect is mediated in part through exercise-induced regulation of maternal physiology and placental development and function. However, the specific mechanisms through which maternal exercise regulates these changes remain to be discovered. We hypothesize that myokines, a collection of peptides and cytokines secreted from contracting skeletal muscles during exercise, may be an important missing link in the story. Myokines are known to reduce inflammation, improve metabolism and enhance macronutrient transporter expression and activity in various tissues of nonpregnant individuals. Little research to date has focused on the specific roles of the myokine secretome in the context of pregnancy; however, it is likely that myokines secreted from exercising skeletal muscles may modulate the maternal milieu and directly impact the vital organ of pregnancy—the placenta. In the current review, data in strong support of this potential role of myokines will be presented, suggesting myokine secretion as a key mechanism through which maternal exercise optimizes fetal growth trajectories. It is clear that further research is warranted in this area, as knowledge of the biological roles of myokines in the context of pregnancy would better inform clinical recommendations for exercise during pregnancy and contribute to the development of important therapeutic interventions.

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