CURES Seminar: Environment, Placenta, and Brain on Neurodevelopmental Outcomes"
This event is in the past.
The Center for Urban Responses to Environmental Stressors (CURES) presents a Wednesday afternoon seminar series on December 4, 2019 from 12:30 to 1:30 p.m. at the IBio Building in Seminar Room 1D, located at 6135 Woodward Ave. The seminar is free and open to the entire University community.
The guest speaker will be Hae-Ryung Park, Ph.D., Postdoctoral Research Fellow of the Department of Molecular and Integrative Physiological Sciences at Harvard University. Dr. Park will present "Environment, Placenta, and Brain on Neurodevelopmental Outcomes".
Dr. Park received both a Bachelors of Science and Masters of Science in Biotechnology from Yonsei University and a Doctorate in Toxicology from the University of Michigan. Her research interests include identifying new targets susceptible to environmental pertubation in relevance with neurodevelopment or neurodegenerative diseases by utilizing functional genetics/genomics (RNAi and CRISPR screens and Next-Generation sequencing), and molecular benchwork.
Disruption of neurodevelopment and cognitive function early in life due to environmental exposures can have lifelong impacts. The unique susceptibility of early brain development may be explained, in part, by the environmental impact on neural stem cells. However, the molecular mechanisms by which environmental factors impact neural stem cell function and early brain development remain poorly understood. Moreover, there are few studies on the inter-relationships between neurotoxicants and the placenta and their roles in fetal neuroprogramming. To fill these knowledge gaps, I propose a highly integrative study combining the state of art methods, molecular mechanistic studies, human genetic epidemiology in children. As a part of this study, we recently performed a genome-wide CRISPR screeen to identify novel suppressors of arsenic (As) -induced endoplasmic reticulum (ER) stress and cell death. Among top hits from the screen, we showed that miR-124 downregulated the IRE1 branch of the ER stress pathway by directly targeting the IRE1 gene. We further showed that miR-124 protects against As-toxicity in neural stem cells and miR-124 genetic polymorphism is associated with neurodevelopmental outcomes in children. Our study implicates As-induced ER stress as a crucial mechanism for the detrimental effects of As on neural cell function and neurodevelopment and identifies miR-124 as a potential preventative and therapeutic target against detrimental effects of As exposure in children. Future studies will directly address the important mechanistic question about the critical susceptibility of early brain development to metal expsoure. I will also explore the unique yet less studied role of the placenta in regulating neural stem cell functions and metal-induced neurotoxicity. The long-term goal of this study is to contribute to the development of novel preventative and therapeutic strategies for metal-related neurodevelopmental pathologies.