Maja Jagodic´s research group

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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.

Research projects

  •     Epigenetic mechanisms of heritable risk factors

Epigenetic landscape of inflammatory cells

  •     A role of micro RNAs in neuroinflammation
  •     DNA methylation of multiple sclerosis lesions
  •     DNA methylation of cell mediators in multiple sclerosis and animal models

Factors that control epigenetic states

  •     Vitamin D induced epigenetic changes
  •     Genetic control of epigenetic state

Selected publications

Next-generation sequencing identifies microRNAs that associate with pathogenic autoimmune neuroinflammation in rats.
Bergman P, James T, Kular L, Ruhrmann S, Kramarova T, Kvist A, et al
J. Immunol. 2013 Apr;190(8):4066-75

An evaluation of analysis pipelines for DNA methylation profiling using the Illumina HumanMethylation450 BeadChip platform.
Marabita F, Almgren M, Lindholm M, Ruhrmann S, Fagerström-Billai F, Jagodic M, et al
Epigenetics 2013 Mar;8(3):333-46

TNF production in macrophages is genetically determined and regulates inflammatory disease in rats.
Gillett A, Marta M, Jin T, Tuncel J, Leclerc P, Nohra R, et al
J. Immunol. 2010 Jul;185(1):442-50

A role for VAV1 in experimental autoimmune encephalomyelitis and multiple sclerosis.
Jagodic M, Colacios C, Nohra R, Dejean A, Beyeen A, Khademi M, et al
Sci Transl Med 2009 Dec;1(10):10ra21

Somatically acquired hypomethylation of IGF2 in breast and colorectal cancer.
Ito Y, Koessler T, Ibrahim A, Rai S, Vowler S, Abu-Amero S, et al
Hum. Mol. Genet. 2008 Sep;17(17):2633-43

Group members

Ewoud EwingGraduate Student
Maja JagodicSenior researcher
Maja JagodicResearch team leader
Lara KularPostdoc
Eliane PiketResearch assistant
Sabrina RuhrmannResearch assistant on study grant
Sabrina RuhrmannGraduate Student
Galina ZheleznyakovaPostdoc