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Association of uterine fibroids with birthweight and gestational age.
Zhao SK, Wu P, Jones SH, Torstenson ES, Hartmann KE, Velez Edwards DR
(2020) Ann Epidemiol 50: 35-40.e2
MeSH Terms: Adult, Birth Weight, Cohort Studies, Female, Fetal Development, Gestational Age, Humans, Leiomyoma, Pregnancy, Prospective Studies, Ultrasonography, Uterine Neoplasms
Show Abstract · Added August 5, 2020
PURPOSE - To determine if fibroids or their characteristics are associated with birthweight and/or gestational age, and to assess the impact of race or ethnicity.
METHODS - Right from the Start (2000-2012) is a prospective cohort that enrolled women from the southern US in early pregnancy. Transvaginal ultrasounds were used to measure fibroid characteristics and confirm gestational age. Date of birth and birthweight were obtained from vital or medical records. We assessed whether fibroid presence, number, type, and volume were associated with birthweight and/or gestational age using multivariate analysis of covariance, accounting for a priori confounders.
RESULTS - Among 3926 women, 416 had one or more fibroids. Mean infant birthweight and gestational age were similar among women with and without fibroids. When adjusting for race or ethnicity, all associations were attenuated. Overall, women with and without fibroids had infants of similar birthweight (-20 grams, 95% confidence interval [CI] -77, 36) and gestational age (0.4 days, 95% CI -0.9, 1.8). Women with three or more fibroids were more likely to have lighter infants (-201 grams, 95% CI -345, -58).
CONCLUSIONS - Race or ethnicity substantially confounds the associations. The clinical belief that uterine fibroids impair fetal growth is supported only by a significant decrease in birthweight for women with multiple fibroids.
Copyright © 2020 Elsevier Inc. All rights reserved.
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12 MeSH Terms
Sex modifies placental gene expression in response to metabolic and inflammatory stress.
Barke TL, Money KM, Du L, Serezani A, Gannon M, Mirnics K, Aronoff DM
(2019) Placenta 78: 1-9
MeSH Terms: Animals, Diabetes, Gestational, Diet, High-Fat, Female, Fetal Development, Fetus, Gene Expression, Inflammation, Male, Mice, Mice, Inbred C57BL, Obesity, Placenta, Pregnancy, Pregnancy Complications, Sex Characteristics, Stress, Physiological, Transcriptome
Show Abstract · Added April 15, 2019
INTRODUCTION - Metabolic stress (e.g., gestational diabetes mellitus (GDM) and obesity) and infections are common during pregnancy, impacting fetal development and the health of offspring. Such antenatal stresses can differentially impact male and female offspring. We sought to determine how metabolic stress and maternal immune activation (MIA), either alone or in combination, alters inflammatory gene expression within the placenta and whether the effects exhibited sexual dimorphism.
METHODS - Female C57BL/6 J mice were fed a normal diet or a high fat diet for 6 weeks prior to mating, with the latter diet inducing a GDM phenotype during pregnancy. Dams within each diet group at gestational day (GD) 12.5 received either an intraperitoneal injection of the viral mimic, polyinosinic:polycytidylic acid (poly(I:C)) or saline. Three hours post injection; placentae were collected and analyzed for changes in the expression of 248 unique immune genes.
RESULTS - Placental immune gene expression was significantly altered by GDM, MIA and the combination of the two (GDM+MIA). mRNA expression was generally lower in placentae of mice exposed to GDM alone compared with the other experimental groups, while mice exposed to MIA exhibited the highest transcript levels. Notably, fetal/placental sex influenced the responses of many immune genes to both metabolic and inflammatory stress.
DISCUSSION - GDM and MIA provoke inflammatory responses within the placenta and such effects exhibit sexual dimorphism. The combination of these stressors impacts the placenta differently than either condition alone. These findings may help explain sexual dimorphism observed in adverse pregnancy outcomes in human offspring exposed to similar stressors.
Copyright © 2019. Published by Elsevier Ltd.
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Epithelial-Derived Inflammation Disrupts Elastin Assembly and Alters Saccular Stage Lung Development.
Benjamin JT, van der Meer R, Im AM, Plosa EJ, Zaynagetdinov R, Burman A, Havrilla ME, Gleaves LA, Polosukhin VV, Deutsch GH, Yanagisawa H, Davidson JM, Prince LS, Young LR, Blackwell TS
(2016) Am J Pathol 186: 1786-1800
MeSH Terms: Animals, Blotting, Western, Elastin, Epithelium, Fetal Development, Humans, Immunohistochemistry, Infant, Newborn, Infant, Premature, Inflammation, Lung, Mice, Mice, Transgenic, Microscopy, Electron, Transmission, Models, Animal, NF-kappa B, Real-Time Polymerase Chain Reaction
Show Abstract · Added February 3, 2017
The highly orchestrated interactions between the epithelium and mesenchyme required for normal lung development can be disrupted by perinatal inflammation in preterm infants, although the mechanisms are incompletely understood. We used transgenic (inhibitory κB kinase β transactivated) mice that conditionally express an activator of the NF-κB pathway in airway epithelium to investigate the impact of epithelial-derived inflammation during lung development. Epithelial NF-κB activation selectively impaired saccular stage lung development, with a phenotype comprising rapidly progressive distal airspace dilation, impaired gas exchange, and perinatal lethality. Epithelial-derived inflammation resulted in disrupted elastic fiber organization and down-regulation of elastin assembly components, including fibulins 4 and 5, lysyl oxidase like-1, and fibrillin-1. Fibulin-5 expression by saccular stage lung fibroblasts was consistently inhibited by treatment with bronchoalveolar lavage fluid from inhibitory κB kinase β transactivated mice, Escherichia coli lipopolysaccharide, or tracheal aspirates from preterm infants exposed to chorioamnionitis. Expression of a dominant NF-κB inhibitor in fibroblasts restored fibulin-5 expression after lipopolysaccharide treatment, whereas reconstitution of fibulin-5 rescued extracellular elastin assembly by saccular stage lung fibroblasts. Elastin organization was disrupted in saccular stage lungs of preterm infants exposed to systemic inflammation. Our study reveals a critical window for elastin assembly during the saccular stage that is disrupted by inflammatory signaling and could be amenable to interventions that restore elastic fiber assembly in the developing lung.
Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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GLI3 Links Environmental Arsenic Exposure and Human Fetal Growth.
Winterbottom EF, Fei DL, Koestler DC, Giambelli C, Wika E, Capobianco AJ, Lee E, Marsit CJ, Karagas MR, Robbins DJ
(2015) EBioMedicine 2: 536-43
MeSH Terms: Adolescent, Adult, Arsenic, Birth Weight, Child Health, Environmental Exposure, Female, Fetal Development, Gene Expression Profiling, Groundwater, Humans, Kruppel-Like Transcription Factors, Maternal Exposure, Middle Aged, Nerve Tissue Proteins, Octamer Transcription Factor-3, Placenta, Pregnancy, Prenatal Exposure Delayed Effects, Signal Transduction, Water Pollutants, Chemical, Water Pollution, Young Adult, Zinc Finger Protein Gli3
Show Abstract · Added November 2, 2015
Although considerable evidence suggests that in utero arsenic exposure affects children's health, these data are mainly from areas of the world where groundwater arsenic levels far exceed the World Health Organization limit of 10 μg/L. We, and others, have found that more common levels of in utero arsenic exposure may also impact children's health. However, the underlying molecular mechanisms are poorly understood. To address this issue, we analyzed the expression of key developmental genes in fetal placenta in a birth cohort of women using unregulated water supplies in a US region with elevated groundwater arsenic. We identified several genes whose expression associated with maternal arsenic exposure in a fetal sex-specific manner. In particular, expression of the HEDGEHOG pathway component, GLI3, in female placentae was both negatively associated with arsenic exposure and positively associated with infant birth weight. This suggests that modulation of GLI3 in the fetal placenta, and perhaps in other fetal tissues, contributes to arsenic's detrimental effects on fetal growth. We showed previously that arsenic-exposed NIH3T3 cells have reduced GLI3 repressor protein. Together, these studies identify GLI3 as a key signaling node that is affected by arsenic, mediating a subset of its effects on developmental signaling and fetal health.
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Developmental consequences of fetal exposure to drugs: what we know and what we still must learn.
Ross EJ, Graham DL, Money KM, Stanwood GD
(2015) Neuropsychopharmacology 40: 61-87
MeSH Terms: Analgesics, Opioid, Animals, Brain, Central Nervous System Stimulants, Female, Fetal Development, Humans, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Substance-Related Disorders
Show Abstract · Added January 20, 2015
Most drugs of abuse easily cross the placenta and can affect fetal brain development. In utero exposures to drugs thus can have long-lasting implications for brain structure and function. These effects on the developing nervous system, before homeostatic regulatory mechanisms are properly calibrated, often differ from their effects on mature systems. In this review, we describe current knowledge on how alcohol, nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) produce alterations in neurodevelopmental trajectory. We focus both on animal models and available clinical and imaging data from cross-sectional and longitudinal human studies. Early studies of fetal exposures focused on classic teratological methods that are insufficient for revealing more subtle effects that are nevertheless very behaviorally relevant. Modern mechanistic approaches have informed us greatly as to how to potentially ameliorate the induced deficits in brain formation and function, but conclude that better delineation of sensitive periods, dose-response relationships, and long-term longitudinal studies assessing future risk of offspring to exhibit learning disabilities, mental health disorders, and limited neural adaptations are crucial to limit the societal impact of these exposures.
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Fetal, maternal, and placental sources of serotonin and new implications for developmental programming of the brain.
Bonnin A, Levitt P
(2011) Neuroscience 197: 1-7
MeSH Terms: Animals, Brain, Female, Fetal Development, Fetus, Humans, Mice, Neurogenesis, Placenta, Pregnancy, Serotonin
Show Abstract · Added April 17, 2013
In addition to its role in neurotransmission, embryonic serotonin (5-HT) has been implicated in the regulation of neurodevelopmental processes. For example, we recently showed that a subset of 5-HT1-receptors expressed in the fetal forebrain mediate a serotonergic modulation of thalamocortical axons response to axon guidance cues, both in vitro and in vivo. This influence of 5-HT signaling on fetal brain wiring raised important questions regarding the source of the ligand during pregnancy. Until recently, it was thought that 5-HT sources impacting brain development arose from maternal transport to the fetus, or from raphe neurons in the brainstem of the fetus. Using genetic mouse models, we uncovered previously unknown differences in 5-HT accumulation between the fore- and hindbrain during early and late fetal stages, through an exogenous source of 5-HT. Using additional genetic strategies, a new technology for studying placental biology ex vivo, and direct manipulation of placental neosynthesis, we investigated the nature of this exogenous source and uncovered a placental 5-HT synthetic pathway from a maternal tryptophan precursor, in both mice and humans. These results implicate a new, direct role for placental metabolic pathways in modulating fetal brain development and suggest an important role for maternal-placental-fetal interactions and 5-HT in the fetal programming of adult mental disorders.
Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
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11 MeSH Terms
Segregation of mtDNA throughout human embryofetal development: m.3243A>G as a model system.
Monnot S, Gigarel N, Samuels DC, Burlet P, Hesters L, Frydman N, Frydman R, Kerbrat V, Funalot B, Martinovic J, Benachi A, Feingold J, Munnich A, Bonnefont JP, Steffann J
(2011) Hum Mutat 32: 116-25
MeSH Terms: DNA, Mitochondrial, Embryonic Development, Female, Fetal Development, Gene Dosage, Humans, MELAS Syndrome, Models, Genetic, Mutation, Pregnancy, Prenatal Diagnosis
Show Abstract · Added December 12, 2013
Mitochondrial DNA (mtDNA) mutations cause a wide range of serious diseases with high transmission risk and maternal inheritance. Tissue heterogeneity of the heteroplasmy rate ("mutant load") accounts for the wide phenotypic spectrum observed in carriers. Owing to the absence of therapy, couples at risk to transmit such disorders commonly ask for prenatal (PND) or preimplantation diagnosis (PGD). The lack of data regarding heteroplasmy distribution throughout intrauterine development, however, hampers the implementation of such procedures. We tracked the segregation of the m.3243A>G mutation (MT-TL1 gene) responsible for the MELAS syndrome in the developing embryo/fetus, using tissues and cells from eight carrier females, their 38 embryos and 12 fetuses. Mutant mtDNA segregation was found to be governed by random genetic drift, during oogenesis and somatic tissue development. The size of the bottleneck operating for m.3243A>G during oogenesis was shown to be individual-dependent. Comparison with data we achieved for the m.8993T>G mutation (MT-ATP6 gene), responsible for the NARP/Leigh syndrome, indicates that these mutations differentially influence mtDNA segregation during oogenesis, while their impact is similar in developing somatic tissues. These data have major consequences for PND and PGD procedures in mtDNA inherited disorders.
© 2010 Wiley-Liss, Inc.
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A population-based case-control study of fetal growth, gestational age, and maternal breast cancer.
Nechuta S, Paneth N, Pathak DR, Gardiner J, Copeland G, Velie EM
(2010) Am J Epidemiol 172: 962-70
MeSH Terms: Adult, Birth Weight, Breast Neoplasms, Carcinoma, Ductal, Breast, Carcinoma, Lobular, Case-Control Studies, Female, Fetal Development, Gestational Age, Humans, Middle Aged, Pregnancy, Risk Factors, Socioeconomic Factors
Show Abstract · Added September 9, 2015
Fetal growth or gestational age in a woman's pregnancies may modify pregnancy-related breast cancer risk, yet studies of these exposures are few. The authors conducted a population-based case-control study among parous Michigan women aged ≤50 years using linked Michigan Cancer Registry (1985-2004) and Michigan livebirth records (1978-2004). Breast cancer cases (n = 7,591) were matched 1:4 to controls (n = 28,382) on maternal birth year and race. Using conditional logistic regression, the authors examined the associations of gestational age (in weeks) and fetal growth (defined using birth weight percentiles for gestational age) in first and last births with breast cancer risk. Having a small-for-gestational-age or large-for-gestational-age infant at a maternal first or last birth was not associated with breast cancer risk, but having a small-for-gestational-age infant at a last birth at ≥30 years modestly reduced risk: odds ratio = 0.82 (95% confidence interval: 0.68, 0.98). First delivery at <32 or >41 weeks also modestly reduced risk: odds ratio = 0.80 (95% confidence interval: 0.62, 1.04) or 0.92 (95% confidence interval: 0.85, 0.99), respectively. In the largest case-control study to date, fetal growth was not associated with overall breast cancer risk in women aged ≤50, and there was some evidence for reduced breast cancer risk for early or late gestational age in first births only.
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14 MeSH Terms
Polymorphisms in maternal and fetal genes encoding for proteins involved in extracellular matrix metabolism alter the risk for small-for-gestational-age.
Edwards DR, Romero R, Kusanovic JP, Hassan SS, Mazaki-Tovi S, Vaisbuch E, Kim CJ, Erez O, Chaiworapongsa T, Pearce BD, Bartlett J, Friel LA, Salisbury BA, Anant MK, Vovis GF, Lee MS, Gomez R, Behnke E, Oyarzun E, Tromp G, Menon R, Williams SM
(2011) J Matern Fetal Neonatal Med 24: 362-80
MeSH Terms: Adult, Case-Control Studies, Extracellular Matrix, Female, Fetal Development, Fetal Growth Retardation, Fetus, Genetic Predisposition to Disease, Humans, Infant, Newborn, Infant, Small for Gestational Age, Male, Maternal-Fetal Relations, Metabolic Networks and Pathways, Mothers, Multifactor Dimensionality Reduction, Polymorphism, Single Nucleotide, Proteins, Risk Factors, Young Adult
Show Abstract · Added February 22, 2016
OBJECTIVE - To examine the association between maternal and fetal genetic variants and small-for-gestational-age (SGA).
METHODS - A case-control study was conducted in patients with SGA neonates (530 maternal and 436 fetal) and controls (599 maternal and 628 fetal); 190 candidate genes and 775 SNPs were studied. Single-locus, multi-locus and haplotype association analyses were performed on maternal and fetal data with logistic regression, multifactor dimensionality reduction (MDR) analysis, and haplotype-based association with 2 and 3 marker sliding windows, respectively. Ingenuity pathway analysis (IPA) software was used to assess pathways that associate with SGA.
RESULTS - The most significant single-locus association in maternal data was with a SNP in tissue inhibitor of metalloproteinase 2 (TIMP2) (rs2277698 OR = 1.71, 95% CI [1.26-2.32], p = 0.0006) while in the fetus it was with a SNP in fibronectin 1 isoform 3 preproprotein (FN1) (rs3796123, OR = 1.46, 95% CI [1.20-1.78], p = 0.0001). Both SNPs were adjusted for potential confounders (maternal body mass index and fetal sex). Haplotype analyses resulted in associations in α 1 type I collagen preproprotein (COL1A1, rs1007086-rs2141279-rs17639446, global p = 0.006) in mothers and FN1 (rs2304573-rs1250204-rs1250215, global p = 0.045) in fetuses. Multi-locus analyses with MDR identified a two SNP model with maternal variants collagen type V α 2 (COL5A2) and plasminogen activator urokinase (PLAU) predicting SGA outcome correctly 59% of the time (p = 0.035).
CONCLUSIONS - Genetic variants in extracellular matrix-related genes showed significant single-locus association with SGA. These data are consistent with other studies that have observed elevated circulating fibronectin concentrations in association with increased risk of SGA. The present study supports the hypothesis that DNA variants can partially explain the risk of SGA in a cohort of Hispanic women.
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Dynamic patterning at the pylorus: formation of an epithelial intestine-stomach boundary in late fetal life.
Li X, Udager AM, Hu C, Qiao XT, Richards N, Gumucio DL
(2009) Dev Dyn 238: 3205-17
MeSH Terms: Animals, Embryo, Mammalian, Female, Fetal Development, Gastric Mucosa, Gene Expression Profiling, Gestational Age, Intestinal Mucosa, Intestines, Kruppel-Like Transcription Factors, Lac Operon, Mice, Mice, Inbred C57BL, Mice, Transgenic, Oligonucleotide Array Sequence Analysis, Pregnancy, Pylorus, Stomach, Zinc Finger Protein GLI1
Show Abstract · Added June 23, 2012
In the adult mouse, distinct morphological and transcriptional differences separate stomach from intestinal epithelium. Remarkably, the epithelial boundary between these two organs is literally one cell thick. This discrete junction is established suddenly and precisely at embryonic day (E) 16.5, by sharpening a previously diffuse intermediate zone. In the present study, we define the dynamic transcriptome of stomach, pylorus, and intestinal tissues between E14.5 and E16.5. We show that establishment of this boundary is concomitant with the induction of over a thousand genes in intestinal epithelium, and these gene products provide intestinal character. Hence, we call this process intestinalization. We identify specific transcription factors (Hnf4 gamma, Creb3l3, and Tcfec) and examine signaling pathways (Hedgehog and Wnt) that may play a role in this process. Finally, we define a unique expression domain at the pylorus itself and detect novel pylorus-specific patterns for the transcription factor Gata3 and the secreted protein nephrocan.
(c) 2009 Wiley-Liss, Inc.
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