Anastasia N Freedman1, Lauren A Eaves1,2, Julia E Rager1,3,2, Noemi Gavino-Lopez1, Lisa Smeester1,2, Jacqueline Bangma1,2, Hudson P Santos2,4, Robert M Joseph5, Karl Ck Kuban6, Thomas Michael O'Shea7, Rebecca C Fry1,3,2. 1. Department of Environmental Sciences & Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC 27599, USA. 2. Institute for Environmental Health Solutions, University of North Carolina, Chapel Hill, NC 27599, USA. 3. Curriculum in Toxicology & Environmental Medicine, School of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA. 4. School of Nursing and Health Studies, University of Miami, Coral Gables, FL 33124, USA. 5. Department of Anatomy & Neurobiology, Boston University School of Medicine, Boston, MA 02118, USA. 6. Department of Pediatrics, Division of Child Neurology, Boston Medical Center, Boston, MA 02118, USA. 7. Department of Pediatrics, School of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.
Abstract
Aim: The placenta-brain axis reflects a developmental linkage where disrupted placental function is associated with impaired neurodevelopment later in life. Placental gene expression and the expression of epigenetic modifiers such as miRNAs may be tied to these impairments and are understudied. Materials & methods: The expression levels of mRNAs (n = 37,268) and their targeting miRNAs (n = 2083) were assessed within placentas collected from the ELGAN study cohort (n = 386). The ELGAN adolescents were assessed for neurocognitive function at age 10 and the association with placental mRNA/miRNAs was determined. Results: Placental mRNAs related to inflammatory and apoptotic processes are under miRNA control and associated with cognitive impairment at age 10. Conclusion: Findings highlight key placenta epigenome-brain relationships that support the developmental origins of health and disease hypothesis.
Aim: The placenta-brain axis reflects a developmental linkage where disrupted placental function is associated with impaired neurodevelopment later in life. Placental gene expression and the expression of epigenetic modifiers such as miRNAs may be tied to these impairments and are understudied. Materials & methods: The expression levels of mRNAs (n = 37,268) and their targeting miRNAs (n = 2083) were assessed within placentas collected from the ELGAN study cohort (n = 386). The ELGAN adolescents were assessed for neurocognitive function at age 10 and the association with placental mRNA/miRNAs was determined. Results: Placental mRNAs related to inflammatory and apoptotic processes are under miRNA control and associated with cognitive impairment at age 10. Conclusion: Findings highlight key placenta epigenome-brain relationships that support the developmental origins of health and disease hypothesis.
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