Dataset Information

Prenatal Exposure to Metals Alters the Placental Inflammatory Proteome in a Sex-Dependent Manner in Extremely Low Gestational Age Newborns

ABSTRACT: Prenatal exposure to toxic metals is associated with altered placental function and adverse health outcomes. The underlying mechanisms linking in utero toxic metal exposures with later-in-life health remain unclear, though placental inflammation is posited as a potential driver. The aim of this study was to evaluate whether in utero metals presence is associated with sex-specific changes in placental protein expression. We hypothesized that sex-specific patterns of metal-associated placental protein expression would be observed, and metals presence would be positively associated with the altered expression of inflammation-associated pathways Using samples banked from the Extremely Low Gestational Age Newborn Study (ELGAN), umbilical cord tissue samples were analyzed via ICP-MS/MS for trace elements, and placental samples underwent a global untargeted proteomics analysis via LC-MS/MS. This work highlights the linkage between prenatal metals exposure and an altered placental proteome, revealing that metals in cord tissue were associated with largely distinct differences in placental protein expression, in a sexually-dimorphic manner.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Placenta

SUBMITTER: Anastasia Freedman

LAB HEAD: Rebecca Fry

PROVIDER: PXD041694 | Pride | 2023-10-24

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20210223_Lumos_PC751-pooled-1.raw	Raw
	20210223_Lumos_PC751_1-1.raw	Raw
	20210223_Lumos_PC751_1-10.raw	Raw
	20210223_Lumos_PC751_1-11.raw	Raw
	20210223_Lumos_PC751_1-12.raw	Raw

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Prenatal Metal Exposure Alters the Placental Proteome in a Sex-Dependent Manner in Extremely Low Gestational Age Newborns: Links to Gestational Age.

Freedman Anastasia N AN Roell Kyle K Engwall Eiona E Bulka Catherine C Kuban Karl C K KCK Herring Laura L Mills Christina A CA Parsons Patrick J PJ Galusha Aubrey A O'Shea Thomas Michael TM Fry Rebecca C RC

International journal of molecular sciences 20231007 19

Prenatal exposure to toxic metals is associated with altered placental function and adverse infant and child health outcomes. Adverse outcomes include those that are observed at the time of birth, such as low birthweight, as well as those that arise later in life, such as neurological impairment. It is often the case that these adverse outcomes show sex-specific responses in relation to toxicant exposures. While the precise molecular mechanisms linking in utero toxic metal exposures with later-i ...[more]

PMID: 37834424

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Project description:Background: Maternal smoking during pregnancy is a major risk factor for adverse health outcomes. The main objective of the study was to assess the impact of in utero tobacco exposure on DNA methylation in children born at term with appropriate weight at birth. Methods: Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood (for methylation arrays) and maternal peripheral venous blood (for cotine level measurement) were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood. Results: The maternal plasmatic cotinine levels ranged from 10.70-115.40 ng/ml in the exposed group to 0-0.59 ng/ml in the non-exposed group. After adjusting for multiple comparisons in 427102 probes, statistically significant differences for 31 CpG sites, associated to 25 genes were observed. There was a greater than expected proportion of statistically-significant loci located in CpG islands (FisherM-bM-^@M-^Ys exact test, p=0.029) and of those CpG islands, 90.3% exhibit higher methylation levels in the exposed group. The most striking and significant CpG site, cg05727225, is located in the chromosome 11p15.4, within the adrenomedullin gene. Conclusions: In utero tobacco exposure, even in the absence of fetal growth restriction, may alter the epigenome, contributing to global DNA hypomethylation. Therefore, DNA status can be used as a biomarker of prenatal insults. Considering the possibility to reverse epigenetic modifications, a window of opportunity exists to change the programmed chronic disease. Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood.