The extracellular matrix (ECM) is a key player in complex processes such as organogenesis, organ function and tissue repair by integrating control of cell adhesion, proliferation, migration, survival, mechanotransduction and differentiation. The ECM is also central in establishment and maintenance of stem cell niches that sustain organ function in the adult.
The importance of ECM in homeostasis is manifested by the vast number of diseases that are caused by abnormalities in cell-ECM interplay encompassing ECM constituents, their cellular receptors and the signals whose activity and transduction the ECM controls.
The CoE of Cell-ECM Research aims to understand how cell-ECM interplay and the ECM microenvironments contribute to tissue development and homeostasis as well as how disruption of these essential conditions and interactions influence the integrity of tissues and development of malignancies. The goal is to understand the dialogue between cells and the extracellular matrix, a process that is necessary for the formation and normal function of organs and blood vessels, as well as in cancers and other types of diseases. The CoE is also interested in exploring the functions of stem cells in the processes of renewal and differentiation. The new understanding gained from these studies will lead to improved diagnostics and treatments during our current CoE term.
The specific aims are to study:
- how regulation of organ development is achieved by Wingless and hypoxia signaling and by the properties of ECM molecules and their receptors.
- how vascular morphogenesis and functions are regulated by endothelial cell-ECM interactions and hypoxia signaling.
- how stem cell fate is controlled by cell-ECM interactions.
- how tissue integrity and mechanotransduction are regulated by specific ECM constituents, their post-translational modifications and the hypoxia response.
- how malignant processes triggered by genetic and epigenetic lesions and molecular dysfunction both cause and are influenced by changes in cell-ECM interactions.
Last updated: 22.6.2016