Multi-Omic Data Illuminates the Placenta’s Role as a Mediator Between Prenatal EDC Exposures and Preterm Birth

Key Takeaways: Preterm birth is one of the leading causes of infant morbidity and is associated with increased birth defects and impaired fetal development. Prenatal exposure to Endocrine Disrupting Chemicals (EDCs) has is positively associated with spontaneous preterm birth (sPTB) in epidemiological studies, and have been shown to alter placental growth and proliferation in vitro. We have used placental transcriptomic data (microRNA and mRNA) to reveal shared molecular mechanisms. Both prenatal EDC exposure and spontaneous preterm birth are associated with increased expression of genes involved in steroid biosynthesis, and decreased genes involved in placental growth and development, including notch signaling and TGF beta signaling.

Alison Paquette, PhD

Assistant Professor
Center for Developmental Biology
Seattle Children’s Research Institute

Speaker Biography: 

Dr. Paquette received her PhD from Dartmouth College under the mentorship of Dr. Carmen Marsit , then joined the Institute for Systems Biology for her post-doctoral fellowship under the mentorship of Dr. Nathan Price. She joined the faculty at Seattle Childrens Research Institute in 2020 and is a member of the Center of Developmental Biology and Regenerative Medicine. She is an Assistant Professor at UW Medicine in the Department of Pediatrics and has an Adjunct appointment in the Department of Environmental and Occupational Health Sciences. She has worked with the ECHO PATHWAYS and PATHWAYS GAPPS cohorts within ECHO through collaborations with cohort lead Dr. Sheela Sathyanaryana. 

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