Nina Kaminen-Ahola
Group Leader

Department of Medical
Genetics

P.O. Box 63
(Haartmaninkatu 8)
00014 University of Helsinki
Finland

nina.kaminen[at]helsinki.fi

+358 (0)50 4482768

Research

We are interested in the mechanisms by which environmental factors affect fetal development at the initial stages of pregnancy. According to the biological programming hypothesis formulated by the esteemed epidemiologist David Barker, an environmental stimulus at a critical moment during development may have permanent effects on gene function and change the course of the development process.

The mechanisms by which the environment affects fetal development still remain largely unknown. According to research, changes in gene expression brought on by epigenetic changes play a significant role in this process. These epigenetic changes are hereditary factors affecting the regulation of gene function that do not stem from changes in the DNA sequence itself. They can be methyl groups that silence gene function and protein biosynthesis when binding to regulatory regions of genes.

Our research focuses on two very different environmental factors, namely, prenatal alcohol exposure and fertility treatments. We study their possible epigenome-mediated effects on gene regulation and fetal development and, hence, the health and phenotype of the individual.

Effects of alcohol on fetal development

Alcohol ingested by the mother during pregnancy is the single most significant cause of congenital developmental disorders in the Western countries. According to some estimates, at least 600 children are born each year in Finland with alcohol-related birth defects, but since these are challenging to identify, the real figure may be as high as 3,000. A wide spectrum of birth defects comprise fetal alcohol spectrum disorders (FASD), the most serious form of which is fetal alcohol syndrome (FAS). FAS typically involves growth disturbances, distinctive facial features and central nervous system dysfunctions that manifest as learning difficulties and social development disorders of varying degrees.

We study the effect of alcohol on the fetal epigenome with the help of mouse models and a collection of human tissue samples. Our objective is to improve the identification of alcohol-related defects, thus enabling the children to have access to the necessary developmental support as early as possible.

 FAS mouse model

By using genomically identical laboratory mice, we are able to exclude genetic variation and variations in the living environment typical to humans. This allows us to focus on changes in the epigenome. In addition, the mouse model enables us to control the time and duration of the alcohol exposure.

epiFASD – epigenetics of fetal alcohol spectrum disorders

We collect samples from children exposed to alcohol during pregnancy at birth, as well as from their parents and a control group. In order to identify the changes caused by alcohol, we compare the expression of genes, the epigenetic profiles of different cell types, and the growth and development details of children exposed to alcohol during pregnancy to the control group. In addition, we study whether fetal alcohol exposure in humans involves the same mechanisms that we find in our mouse model.

Effects of fertility treatments on fetal development

epiART – epigenetics of assisted reproductive technology

Fertility treatment methods are employed at crucial stages in terms of the formation of the epigenome, namely, the ripening of the oocyte and the early embryonic stage. The purpose of our study is to find whether fertility treatment methods affect gene regulation in the fetus or the placenta, thus affecting the child’s development and subsequent health.