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Inflammatory Signalling Lab

Inflammatory Signalling Lab

Group leader
Annika Meinander, Docent, PhD
Senior Lecturer (Akademilektor)
Cell Biology

Group Members
Anna Aalto, PhD student
Aravind Kumar Mohan, PhD student
Christa Kietz, PhD student
Fanny Sundqvist, PhD student
Gabriela Martinez-Chacon, research fellow
Nadezhda Tsyganova, EDUFI fellow
Sabrina Benoit, MSc student
Jesper Lindholm, MSc student

Contact information

Faculty of Science and Engineering
Cell Biology
BioCity, 2nd floor
Tykistokatu 6
FI-20520 Turku
Finland
Tel. +358 469201699
Tel. internal 215 4602
Email: annika.meinander@ abo.fi

 

Research focus
Diseases involving chronic inflammation, such as inflammatory bowel disease (IBD) are increasing in Finland and worldwide, especially among young people. Apprehensively, IBD such as ulcerative colitis and Crohn’s disease is a major risk factor for colorectal cancer. Similarly, chronic inflammation in the lung epithelia due to asthma or pulmonary disease is associated with lung cancer. My laboratory studies how a protein modification named ubiquitination regulates inflammation in the cells in the intestine and the airways.
As chronic inflammation is caused by defects in regulation of inflammatory signalling, flexible but precise mechanisms are needed to control inflammation-promoting signals in cells. The NF-kappaB family of transcription factors are major mediators of inflammatory gene expression in epithelial tissue during chronic inflammation. Post-translational modifications, such as ubiquitination, increase the possibilities to regulate protein functions, and we aim at controlling inflammatory NF-kappaB activation in intestinal and tracheal epithelia by regulating ubiquitin signalling. We use the fruit fly Drosophila melanogaster as a model to study epithelial inflammation, as it allows us to manipulate and analyse molecule and gene functions in an environment of chronic inflammation. As the signalling pathways regulating ubiquitination and NF-kappaB activation are conserved through evolution, this research will enhance our knowledge of the molecular changes in chronic inflammation, and may lead to discovery of new drug targets and diagnostic markers.

Research environment
The Åbo Akademi University life sciences laboratories are active on the Kupittaa campus together with the life sciences and medical researchers from University of Turku and Turku University Hospital. Research in life sciences at Åbo Akademi University is supported by strong organizations such as BioCity Turku and Health Campus Turku, which strengthen the opportunities for collaboration and innovation on our campus. We also have access to advanced state of the art infrastructure through Turku Bioscience, Turku BioImaging and EuroBioimaging. We are also part of the ÅAU Center of Excellence project CellMech (Center of Excellence in Cellular Mechanostasis).

 

Ongoing Projects

Targeting ubiquitin signaling in chronic inflammation

Targeting chronic intestinal inflammation by interfering with ubiquitin signaling

Caspase-mediated regulation of ubiquitination in inflammatory signaling in Drosophila

Intermediate filament networks in Drosophila epithelial tissues

Mechanical forces regulating tissue function and repair (CellMech)

Funding

The Academy of Finland
The Sigrid Jusélius Foundation
The Magnus Ehrnrooth Foundation
The Liv och Hälsa Foundation
The Doctoral Network of Molecular Biosciences (MolBio)

 

Selected publications

Aalto A, Mohan AK, Schwintzer L, Kupka S, Walczak H, Broemer M, Meinander A. (2019) M1-linked ubiquitination by LUBEL is required for inflammatory responses to oral infection in Drosophila. Cell Death Differ. Ahead of print, doi: 10.1038/s41418-018-0164-x

Kietz C, Pollari V, Meinander A. (2018) Generating Germ-Free Drosophila toStudy Gut-Microbe Interactions: Protocol to Rear Drosophila under Axenic Condition. Curr Protoc Toxicol, Ahead of print, doi: 10.1002/cptx.52

Gullmets J, Torvaldson E, Lindqvist J, Imanishi SY, Taimen P, Meinander A*, Eriksson JE*. (2017) Internal epithelia in Drosophila display rudimentary competence to form cytoplasmic networks of transgenic human vimentin. FASEB J. doi:10.1096, *equal contribution

Sahlgren C, Meinander A, Zhang H, Cheng F, Preis M, Xu C, Salminen TA, Toivola D, Abankwa D, Rosling A, Karaman DŞ, Salo-Ahen OMH, Österbacka R, Eriksson JE, Willför S, Petre I, Peltonen J, Leino R, Johnson M, Rosenholm J, Sandler N. (2017) Tailored Approaches in Drug Development and Diagnostics: From Molecular Design to Biological Model Systems. Adv. Healthc. Mater. doi: 10.1002

Meinander A, Runchel C, Tenev T, Chen L, Kim C-H, Ribeiro PS, Broemer M, Leulier F, Zvelebil M, Silverman N and Meier P. (2012) Ubiquitylation of the Initiator Caspase Dredd is Required for Innate Immune Signalling.  EMBO J. 31: 2770-2783.

Rosenholm JM, Meinander A, Peuhu E, Niemi R, Eriksson JE, Sahlgren CM, and Lindén M. (2009) Targeting of porous hybrid silica nanoparticles to cancer cells. ACS Nano. 3: 197-206.

Meinander A, Söderström TS, Kaunisto A, Poukkula M, Sistonen L, and Eriksson JE. (2007) Fever-like hyperthermia controls T-lymphocyte persistence by inducing degradation of c-FLIPshort. J. Immunol. 178: 3944-3953.

Tran SEF, Meinander A, and Eriksson JE. (2004) Instant decisions: transcription-independent control of death receptor-mediated apoptosis. Trends Biochem. Sci. 11: 601-606.

 

Sammanfattning av forskningen på svenska
Sjukdomar som involverar kronisk inflammation, såsom inflammatorisk tarmsjukdom ökar globalt, särskilt bland unga människor. Samtidigt är kroniska tarminflammationer en riskfaktor för tjocktarmscancer. På motsvarande sätt kan kronisk inflammation i luftvägarna förorsakad av astma eller lungsjukdomar förknippas med lungcancer. Mitt laboratorium undersöker hur en proteinmodifikation som kallas ubikvitinering påverkar inflammation i cellerna i tarmen och luftvägarna. Eftersom inflammationssignalering är mycket komplex i däggdjursceller, använder vi bananflugan Drosophila melanogaster som modellorganism i våra studier. Vår forskning kommer att förbättra vår förståelse av hur proteinmodifikationer påverkar inflammationssignalering i cellerna och denna kunskap öppnar möjligheter för upptäckt av nya sätt att detektera och nya läkemedel för att hämma kronisk inflammation

Updated 19.11.2019