Prior to my CASCADE-FELLOWS fellowship, I was associate professor at the Faculty of Biology, the University of Belgrade, Serbia. During my PhD, I worked in a project investigating transcriptional regulation of brown adipose tissue development and hyperplasia.
I am working on my project at the Stem Cell Biology group in the Wolfson Centre for Stem Cells, Tissue Engineering and Modelling (STEM) at the University of Nottingham and Early Life Research Unit at the Queen’ s Medical Centre.
I am interested in molecular mechanisms regulating the differentiation ability of mesenchymal stem cells (MSCs) from different tissues towards brown adipogenic lineages.
Brief description of research project
Fat tissue plays important roles in the control of body processes, from energy storage to inflammation and chronic diseases. There are two types of fat tissue: white adipose tissue (WAT) which stores excess fat, and brown adipose tissue (BAT) which generates heat by burning fat in response to temperature changes. Excess in WAT leads to obesity and associated pathologies, so there is a need for new treatments able to promote BAT rather than WAT.
Recently, it has been shown that a proportion of WAT can become BAT in response to specific conditions. It is therefore possible to target WAT depots and change their properties in order to burn fat rather than store it as a way to combat obesity. In order to identify novel therapies, our project proposes to use human stem cells to test and validate treatments inducing conversion to BAT as a first step towards new clinical applications.
Since I didn’t have any experience of cell culture and in vitro studies, at the beginning of my fellowship I was trained for standard cell culture methods (isolation/growth of mouse/rat/human adult mesenchymal stem cells (MSCs) from different tissue sources, their differentiation and sample preparation for cytochemical, biochemical and molecular methods). MSC cultures from both bone marrow (BM), and brown and white adipose tissue (BAT and WAT, respectively) were characterised and compared for marker expression, growth kinetics and adipogenic differentiation. After methodology validation, I started to investigate new brown adipogenic inducers using mouse MSCs as an in vitro model of differentiation. For the most promising molecules/compounds which we have identified as promising candidates, the precise role and pathway involved in adipogenesis is now being determined. Additionally, changes in gene expression triggered by these new candidates will now be analysed to define the key molecular events involved in the browning process.