# Placental adaptive mechanisms to environmental exposures.

> **NIH NIH R01** · UNIVERSITY OF ILLINOIS AT CHICAGO · 2020 · $348,749

## Abstract

ABSTRACT
The placenta is the gateway between the mother and the developing fetus. Placental dysfunction can impair
fetal growth and induce long-term effects in the progeny, including increased risk for metabolic diseases. The
delicate balance of feto-maternal communication / exchange can be affected by a number of factors including
maternal diet and diseases and / or exposure to endocrine disrupting compounds (EDCs). EDCs are synthetic
or natural chemicals that interfere with the normal function of the endocrine system with some EDCs having
steroidal activity. Fetal exposure to such EDCs can pose a threat to adult well-being. Current policy regulations
are limiting the use of one of such EDCs, bisphenol A (BPA), in the manufacture process of consumer
products. Emergence of new, untested, industrial chemical substitutes such as bisphenol S (BPS), an EDC
with very distinct steroid affinities compared to BPA, are on the rise. Understanding the health risks posed by
emerging EDC exposures is critical. Our preliminary studies using sheep as an in vivo model and in vitro
studies using human cytotrophoblasts demonstrate that BPS exposure alters placental trophoblast function.
BPA does not lead to a similar placental phenotype, highlighting critical and unexplored differences among
bisphenolic EDCs. Our preliminary data suggest that BPS mediates its action via the progesterone receptor
pathway. In our animal model, gestational BPS exposure also impacts fetal size and leads to cardio-metabolic
disruptions. Studies described in this proposal will capitalize on a unique animal model of feto-maternal
communication, primary trophoblast cells and trophoblast cell lines to test a novel hypothesis for the
developmental origin of cardio-metabolic disorders with specific emphasis on understanding the molecular
mechanisms whereby BPS compromises trophoblast function placental function and long-term cardio-
metabolic effects on the progeny.

## Key facts

- **NIH application ID:** 10233182
- **Project number:** 7R01ES027863-04
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **Principal Investigator:** Almudena Veiga-Lopez
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $348,749
- **Award type:** 7
- **Project period:** 2020-11-19 → 2023-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10233182

## Citation

> US National Institutes of Health, RePORTER application 10233182, Placental adaptive mechanisms to environmental exposures. (7R01ES027863-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10233182. Licensed CC0.

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