My Research
DNA methylation in trophoblast cells
Very little is understood about placental development at a molecular level. Placental dysfunction is often associated with pregnancy complications and disruption of epigenetic mechanisms. Studying placental DNA methylation is complicated by the presence of multiple different cell types each with their own unique methylomes.
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Using immunohistochemistry (IHC) and immunofluorescence (IF) we have investigated the localisation of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC), in placenta tissue across gestation and in pregnancy complications. We are currently characterising the 5mC and 5hmC profiles in detail in different trophoblast cell populations.
Long non coding RNAs
We have identified a number of long non-coding RNAs (lncRNAs) that are altered in the placenta across pregnancy. We believe disruptions to these may contribute to common pregnancy complications. We have manipulated the expression of these lncRNAs in trophoblast cells and assessed how they change the cell phenotype.
Molecular characterisation of micronutrients
We use numerous models like cell lines, primary cells and tissue explants to characterise the role of micronutrients and other compounds. We investigate how these compounds impact cell proliferation, apoptosis and other important regulatory pathways.
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Novel plant extracts and human health
In collaboration with several researchers at the University of Adelaide we are looking at the effects of plant extracts on human health and disease. With our increasing global population there is a pressing need for significantly increased plant production as well as the development of novel nutritious food sources which contain high quality nutrients. However, often the less obvious benefits of these alternative food sources have not been thoroughly validated or tested and there is a high likelihood that they also contain valuable therapeutics to improve human health and prevent future disease.
Epigenetics in DOHaD
It is well known that adverse events that occur during early in life can program risk of chronic diseases later in life and the likely mechanism by which this occurs is epigenetics. Using animal models we are investigating how environmental exposures can alter organ development and hence program future disease risk in a sex-specific manner and across multiple generations.