Aims
The analysis of molecular elements involved in the communication between cells is key to understanding human health and disease. Organ development, homeostasis and maintenance are controlled by a large variety of intra-, inter- and extracellular signals that have to be integrated by every cell to achieve properly coordinated cell-specific functions within a multi-cellular organism. Accordingly, disruption of this cellular communication, either by a gain of cell-autonomous functions or by a loss of cell-cell interactions leads to a lack of coordination and to malfunction. The principle that diseases are caused by a failure in cellular communication applies not only to rare monogenetic diseases, but also to widespread diseases such as neurodegenerative and autoimmune diseases, atherosclerosis, or chronic inflammatory diseases. Therefore, an understanding of the molecular physiology of cellular communication is an essential prerequisite for the perception of pathological alterations that lead to certain symptoms. The dissection of pathologically altered cell communication opens the way for specific interference as basis for the functional restoration. In accordance with this principle, most pharmacotherapeutic agents exert their actions by interfering with some aspect of cellular communication, such as hormone receptors and associated signal cascades.
The investigation of inter- or intracellular communication pathways provides intellectual and technical skills that can be employed in highly divergent areas. Even in highly heterogeneous cells, fundamental mechanisms often operate in an analogous manner. For instance, the adipocyte-derived hormone leptin plays a role in the regulation of food intake and in immune responses. It is not only a neuromodulator that governs neuronal firing, but also an immunomodulator involved in, for instance, experimental autoimmune encephalitis, type 1 diabetes, and rheumatoid arthritis. Reverse examples are cytokines of the interleukin-1 family, which are key regulators of immune reactions and inflammation, but which also control neurotransmission and the development of atherosclerosis. Likewise, Toll-like receptors are not only involved in immune responses, but also in atherosclerosis and brain inflammation. The angiogenic peptide vascular endothelial growth factor can be used to treat ischemic diseases following atherosclerosis, but also mediates neuroprotective effects in neurodegenerative diseases. In accordance with the above examples of analogies in cell communication in different tissues, CCHD is not intended to focus on one type of communication, such as synaptic transmission, interleukin signalling, or angiogenesis, but rather provides examples stemming from diverse organ systems. Therefore, graduates of this program will be trained to apply their conceptual expertise not only within the predefined themes of their own theses, but also in topics that go beyond their very own projects.
In agreement with these general considerations, four thematic fields of research have been chosen as focus of CCHD: (1) the neurobiology field, (2) the vascular biology field, (3) the immunology field, and (4) the inflammation field. These four topics are also priority research areas at the MUW. On the following pages, overviews are given for each of these research fields.
