The University of Oslo is closed and the public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Click here to participate in the public defence
Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Dr. James Whiteford, Queen Mary University of London, UK
- Second opponent: Dr. Katalin Dobra, Karolinska Institutet, Sweden
- Third member and chair of the evaluation committee: Professor Kåre-Olav Stensløkken, University of Oslo
Chair of the Defence
Associate Professor Kjetil Wessel Andressen, University Of Oslo
Principal Supervisor
Researcher Cathrine Rein Carlson, University of Oslo
Summary
Remodeling of the heart can lead to heart failure, but molecular mediators of this process are not well understood. Syndecan-4 has previously been identified as a pro-cardiac remodeling factor in a “top-down” approach by screening an in vivo heart failure model. For the present thesis an exploratory “bottom-up” approach was applied. The overall aim was to investigate the interaction partners of syndecan-2 and -4 to learn more about their routes of action in the heart. For syndecan-4 a total of 21 novel and 41 out of 71 previously described interaction partners were found in the heart. Of these, 19 showed an altered binding after aortic banding, an in vivo model of heart failure. One of these was muscle LIM protein (MLP), which is known to translocate into the nucleus during cardiac remodeling and affect gene transcription. Results presented in this thesis support a role for syndecan-4 in the nuclear translocation of MLP. Furthermore, a novel connection between the cytoplasmic domain of syndecan-4 and the adaptor proteins α- and β-parvin was identified and mapped. Syndecan-2 is the closets relative of syndecan-4 and is also expressed in the heart, however very little is known about its role in a cardiac setting. In total 31 novel and 9 out of 41 previously described interaction partners were found for syndecan-2 in the heart. Collectively, our data expand our knowledge of intracellular interactions of syndecan-2 and -4 and shed light on their signalling paths in the heart.
Additional information
Contact the research support staff.