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The association between prenatal alcohol exposure and protein expression in human placenta
Bradley D Holbrook1, Suzy Davies2, Sandra Cano3
1Department of Obstetrics & Gynecology, School of Medicine, University of New Mexico, Albuquerque, New Mexico.
Insights
Prenatal ethanol exposure (PAE) alters placental expression of angiogenesis proteins like VEGFR2 and annexin-A4. These placental biomarkers show potential for identifying fetal development alterations due to PAE.
Area of Science:
- Obstetrics and Gynecology
- Developmental Biology
- Neuroscience
Background:
- Prenatal ethanol exposure (PAE) poses risks for neurobehavioral problems in children.
- Early identification of at-risk infants requires prognostic biomarkers for altered fetal development.
- Placental protein expression is a potential indicator of fetal development influenced by PAE.
Purpose of the Study:
- To investigate if PAE alters the expression of angiogenesis-related proteins and cytokines in human placenta.
- To assess the diagnostic utility of placental biomarkers for PAE.
- To explore the role of these proteins in PAE-induced pathology.
Main Methods:
- Prospective cohort study design.
- PAE ascertained through questionnaires, interviews, and ethanol biomarkers.
- Placental tissue collected post-delivery for protein and cytokine analysis.
Main Results:
- PAE was associated with reduced placental expression of VEGFR2 and annexin-A4.
- VEGFR1 and CCM-3 levels trended downward in the PAE group.
- Trends toward higher TNF-α and IL-13 expression were observed in PAE subjects.
- Placental proteins demonstrated moderate-to-high diagnostic accuracy for PAE, enhanced by combinations.
Conclusions:
- Placental tissue harvesting for prospective PAE protein analysis is feasible.
- Angiogenic and cytokine proteins warrant further investigation for predicting brain development alterations.
- These proteins may play a mechanistic role in PAE-induced pathology.
Background:
The need for earlier recognition of children at risk for neurobehavioral problems associated with prenatal ethanol exposure (PAE) has prompted investigations of biomarkers prognostic for altered fetal development. Here, we examined whether PAE alters the expression of angiogenesis-related proteins and cytokines in human placenta in subjects from an Ethanol, Neurodevelopment, Infant and Child Health prospective cohort.
Methods:
PAE was ascertained by screening questionnaires, Time-line Follow-back interviews and a panel of ethanol biomarkers at two study visits. After delivery, placental tissue samples were collected for protein analysis.
Results:
No significant differences in the prevalence of substance use, demographic or medical characteristics were observed between the No PAE and PAE groups. PAE was associated with significant reductions in placental expression of VEGFR2 and annexin-A4, while the levels of VEGFR1 and CCM-3 trended downward. A trend toward higher expression of the cytokines TNF-α and IL-13 was also observed in the PAE group. Receiver operating characteristic analyses of the data demonstrated a moderate-to-high degree of diagnostic accuracy for individual placental proteins. Combinations of proteins substantially increased their ability to differentiate between PAE and No PAE subjects.
Conclusions:
These results establish the feasibility of harvesting placental tissue for protein analyses of PAE in a prospective manner. In addition, given the importance of vascular remodeling in both placenta and developing brain, the role of angiogenic and cytokine proteins in this process warrants further investigation for their utility for predicting alterations in brain development, as well as their mechanistic role in PAE-induced pathology.
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