Mitic Lab investigates the epigenetic changes in hypoxia and during vascular injury.

We are interested in Polycomb repressive activities in adult vascular tissue homeostasis under physiological & pathological conditions. Polycomb Repressive Complex 2 (PRC2) is a transcriptional repressor regulating early development and it is a known pharmacological target for prevention of cancer progression. The actions of PRC2 are not well investigated in cardiovascular diseases, although some pathologies already benefited from targeted PRC2 inhibition. We identified long non coding RNAs (lncRNAs) that bind PRC2 subunits in endothelial cells and associated them with the vascular diseases. We are also intersecting the chromatin and RNA binding capacities of PRC2 to identify the reglatory mechanisms of relevance for endothelial targets.

Tijana obtained her PhD from the University of Edinburgh in 2010 where she completed a short postdoc at the Endicrinology Unit (Prof J Seckl). She then moved to a successful postdoc at the Bristol Heart Institute (2011-2014) where she was responsible for securing £100,000 in research funding (EFSD and SfE) and have successfully published this work in the best journal in the field, before taking a break from academia. In 2016, Tijana was awarded a highly competitive early career Fellowship from the British Heart Foundation to restart her academic research (BHF, £285,100). In 2019, she was also awarded a teaching Fellowship of the Higher Education Academy. Tijana now leads a research team of a technician and a MSc research student.

With up to 12 years of academic research experience I have worked in both basic and pre-clinical projects in the UK and abroad. I speak three languages and look after 5-year old boy (and a 40+ husband) :)

Tijana Mitic Linkedin Profile

We have identified binding sites within maternally expressed gene (MEG3) lncRNA that interacts with the Polycomb via EZH2 subunit. We have determined common targets for MEG3 and EZH2 candidates in vascular cells and found that they mutually regulate endothelial cell function. This work unravels the new mechanism of how lncRNA can target a transcriptional factor onto a promoter of gene to directly block endothelial cell function.