Exposure and fetal growth-associated miRNA alterations in the human placenta

Matthew A Maccani,Carmen J Marsit

doi:10.1007/s13148-011-0046-2

Matthew A Maccani, Carmen J Marsit

Open Access

https://doi.org/10.1007/s13148-011-0046-2

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Abstract

Researchers have begun to examine epigenetic alterations in the placenta, making key advances in understanding the epigenetic regulatory mechanisms of the placenta that define underlying processes of human development and disease. Examining changes in microRNA (miRNA) expression associated with environmental exposures and fetal growth is providing critical insights into the biology of development, response to in utero exposure, and future disease risk assessment. This review aims to highlight previous studies describing changes in miRNA expression in the human placenta associated with in utero exposure and fetal growth and seeks to assess the future directions in this exciting field of research.

Highlights

Work in the developmental origins of health and disease has shifted to investigating the molecular mechanisms of fetal programming
Maternal cigarette smoking during pregnancy is associated with the downregulation of miR-16, miR-21, and miR-146a in term human placental tissue, and two components of cigarette smoke, nicotine and benzo(a)pyrene, result in the significant dosedependent downregulation of miR-146a in an in vitro model (Maccani et al 2010)
Knowledge of the molecular mechanisms underlying placental gene regulation may be enhanced by identifying miRNA biomarkers for exposure, burden, or risk for disease

Summary

Introduction

Work in the developmental origins of health and disease has shifted to investigating the molecular mechanisms of fetal programming. Avissar-Whiting et al showed that miR-146a is sensitive to dysregulation by bisphenol A exposure in placental cell lines, further suggesting that miR-146a may be especially sensitive to modulation by exposure to these environmental toxicants (Avissar-Whiting et al 2010; Maccani et al 2010) These studies suggest that potentially hazardous environmental toxicants may modulate miRNA expression in the placenta, thereby underscoring the need for future work to better understand the possible downstream effects of toxicantdysregulated miRNA expression in the placenta. 2011), utilizing various long-term gestational exposures and examinations at multiple timepoints in pregnancy, could elaborate on the normal and exposure-modulated roles of miRNA in placenta function Such findings using an in vivo model system may provide key mechanistic data that can further strengthen current epidemiologic association studies

Objectives

Conclusion