Associate Professor Bas Heijmans, Molecular Epidemiology Section, Leiden University Medical Center, The Netherlands “The prenatal epigenome and studies into long-term health”

4 September 2014, 3.28 PM - 4 September 2014, 5.28 PM

ASSOCIATE PROFESSOR BAS HEIJMANS

 Molecular Epidemiology Section, Leiden University Medical Center, The Netherlands

 THURSDAY, 4TH SEPTEMBER, 2014

 1600 – 1700 : SEMINAR ROOM

2nd FLOOR, OAKFIELD HOUSE

“The prenatal epigenome and studies into long-term health”

  

Abstract:

Epigenetic mechanisms, including DNA methylation, are a plausible molecular mediator of the reported association between the prenatal environment and adult health. Supporting empirical evidence in humans, however, remains relatively scarce. The prenatal epigenome may be particularly sensitive to the environment because of the large-scale epigenomic remodeling that occurs during development. This remodeling is relatively well-described for the early mouse embryo, but has not been studied in human development. A genome-wide analysis of DNA methylation dynamics during human fetal development revealed striking differences in the characteristics of regions showing loss and gain of methylation, defined biological roles of dynamic regions and uncovered an overlap with known disease loci. Apart from the need for insight in fundamental biology, new approaches in epigenetic epidemiology are to be developed. To be maximally effective, they should optimally incorporate well-characterized human populations despite their inherent limitations. Prenatal exposure to the Dutch Hunger Winter at the end of World War 2 is a well-documented quasi-experimental setting of malnutrition during gestation. A systematic characterization of DNA methylation differences associated with prenatal famine exposure, indicated their occurrence at regulatory regions, including developmental enhancers, and suggested a link between prenatal malnutrition and epigenetic tuning of processes related to growth and development.

Bas Heijmans

Bas Heijmans studies the role of genomic variation in human disease and ageing. His recent focus is on how the prenatal environment can induce persistent changes in the human epigenome and how these changes may contribute to metabolic disease. This topic fits in his broader research interest to use genome-scale genetic, epigenetic, expression and other molecular data in studying human cardiometabolic disease and ageing. He was trained as a (molecular) biologist and in his human studies he combines the application of medium/high-throughput laboratory techniques with data analysis in the setting of molecular epidemiology.

 

 

ALL WELCOME

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