Epigenetic origins and mechanisms in neuroinflammation
Epigenetics is comprised of stable changes of gene expression inherited from one cell generation to the next without a change in DNA sequence (genetic code). It provides additional and more flexible level of regulation on the top of the genetic code, which can also be modulated by environment.
We are studying how epigenetic mechanisms influence neuroinflammation in humans and experimental models. Due to stability, epigenetic modifications may provide robust and stable biomarkers of disease activity. Due to reversibility, it may be possible to alter unfavorable epigenetic state and treat the disease.
We aim to characterize epigenetic mechanisms underlying neuroinflammation with the prospect of a better understanding chronic inflammatory diseases and developing novel treatments and biomarkers. Epigenetic changes occur in response to internal and external environment and decide the timing and location of gene expression. This is mainly achieved through DNA methylation, histone modifications and action of nuclear factors and non-coding RNAs, which shape the 3D structure of genetic material.
Our focus is on DNA methylation and micro RNAs. We investigate (i) epigenetic inheritance of inflammation, (ii) epigenetic landscape of inflammatory cells and inflamed tissues and (iii) genetic and environmental factors that control epigenetic states.