Dataset Information

Modulation of Placental Gene Expression in Small-for-Gestational-Age Infants.

ABSTRACT: Small-for-gestational-age (SGA) infants are fetuses that have not reached their genetically programmed growth potential. Low birth weight predisposes these infants to an increased risk of developing cardiovascular, metabolic and neurodevelopmental conditions in later life. However, our understanding of how this pathology occurs is currently incomplete. Previous research has focused on understanding the transcriptome, epigenome and bacterial signatures separately. However, we hypothesise that interactions between moderators of gene expression are critical to understanding fetal growth restriction. Through a review of the current literature, we identify that there is evidence of modulated expression/methylation of the placental genome and the presence of bacterial DNA in the placental tissue of SGA infants. We also identify that despite limited evidence of the interactions between the above results, there are promising suggestions of a relationship between bacterial signatures and placental function. This review aims to summarise the current literature concerning fetal growth from multiple avenues and propose a novel relationship between the placental transcriptome, methylome and bacterial signature that, if characterised, may be able to improve our current understanding of the placental response to stress and the aetiology of growth restriction.

SUBMITTER: O'Callaghan JL

PROVIDER: S-EPMC7017208 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Modulation of Placental Gene Expression in Small-for-Gestational-Age Infants.

O'Callaghan Jessica L JL Clifton Vicki L VL Prentis Peter P Ewing Adam A Miller Yvette D YD Pelzer Elise S ES

Genes 20200110 1

Small-for-gestational-age (SGA) infants are fetuses that have not reached their genetically programmed growth potential. Low birth weight predisposes these infants to an increased risk of developing cardiovascular, metabolic and neurodevelopmental conditions in later life. However, our understanding of how this pathology occurs is currently incomplete. Previous research has focused on understanding the transcriptome, epigenome and bacterial signatures separately. However, we hypothesise that int ...[more]

PMID: 31936801

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Project description:To investigate the potential risk factors for small-for-gestational-age (SGA) and appropriate-for-gestational-age (AGA) late-term infants, 100 cases of single full-term SGA infants delivered in the Department of Obstetrics, The First Affiliated Hospital of Chongqing Medical University in 2017 were enrolled as the SGA group. A total of 100 healthy AGA who were born at the same time with the same gestational age were randomly included as the control group. The perinatal and postpartum adverse conditions of the two groups were recorded, and Apgar tests were performed on all newborns at 1 min (T1), 5 min (T2) and 10 min (T3) after birth. A follow-up survey was conducted in all patients at 6 and 12 months of age. At the second follow-up, the development quotient of the children was measured using the Gesell Developmental Schedule, and the perinatal risk factors of SGA were analyzed. The incidence of intrauterine distress, respiratory distress syndrome and infectious disease in the SGA group was significantly higher compared with that in the AGA group (P<0.05). The Apgar scores at T1, T2 and T3 were significantly lower in the SGA group compared with the AGA group (P<0.05). The Apgar score at T1 was lower compared with that at T2 in the SGA group (P<0.05), and the Apgar score at T2 was lower compared with that at T3 (P<0.05). The length of hospital stay in the SGA group was significantly longer compared with that in the AGA group (P<0.05). The development quotient at the 6 and 12th month in the SGA group was significantly lower compared with that in the AGA group (P<0.05). Logistic regression analysis showed that there was no correlation between SGA and maternal age, regardless of firstborn status, neonatal sex, mode of delivery and living environment. SGA was significantly associated with umbilical cord abnormalities, maternal pregnancy-induced hypertension, gestational diabetes, pregnancy infection and intrauterine distress (P<0.05). An abnormal umbilical cord, maternal pregnancy-induced hypertension, gestational diabetes, infection during pregnancy and intrauterine distress are all perinatal risk factors for SGA. Effective interventions are needed in clinical assessment to prevent the occurrence of SGA.

Project description:BackgroundThe placenta is an essential organ that provides nutrients and oxygen to the developing fetus and removes toxic waste products from the fetal circulation. Maintaining placental blood osmotic pressure and blood flow is crucial for viable offspring. The renin-angiotensin system (RAS) in the placenta is a key player in the regulation of maternal-fetal blood flow during pregnancy. Therefore, the aim of this study was to determine if RAS genes are differentially expressed in mid to late gestation in rat placenta.MethodsWhole placental tissue samples from pregnant Sprague Dawley rats at embryonic (E) days 14.25, 15.25, 17.25 and 20 (n = 6 for each gestational age) were used for genome-wide gene expression by microarray. RAS genes with expression differences of >2 fold were further analyzed. Quantitative Real-Time PCR (qPCR) was performed on independent samples to confirm and validate microarray data. Immunohistochemisty and Western blotting were performed on a differentially expressed novel RAS pathway gene (ANPEP).ResultsSix out of 17 genes of the RAS pathway were differentially expressed at different gestational ages. Gene expression of four genes (Angiotensin converting enzyme (Ace), angiotensin converting enzyme 2 (Ace2), membrane metalloendopeptidase (Mme) and angiotensin II receptor 1A (Agtr1a)) were significantly upregulated at E20 whereas two others (Thimet oligopeptidase 1 (Thop1) and Alanyl aminopeptidase (Anpep)) were downregulated at E20 prior to the onset of labour. These changes were confirmed by qPCR. Western blots revealed no overall differences in ANPEP protein expression in the placentae. Immunohistochemical studies, however, indicated that the localization of ANPEP differed at E17.25 and E20 as ANPEP localization in the giant trophoblast cell of the junctional zone was no longer detectable at E20.ConclusionsThe current study investigated the expression of members of the RAS pathway in rat placentae and observed significantly altered expression of 6 RAS genes at 4 gestational ages. These findings present the need for further comprehensive investigation of RAS genes in normal and complicated pregnancies.

Dataset Information

Modulation of Placental Gene Expression in Small-for-Gestational-Age Infants.

Publications

Modulation of Placental Gene Expression in Small-for-Gestational-Age Infants.

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