The Role of CXCR7 in Tissue Fibrosis
Chemokines are small molecules that provide guidance cues for cells during embryonic development on the one hand and are equally critical for the migration of immune cells on the other hand. The CXCL12 - CXCR4 chemokine axis is a long-known central player in the immune system during steady state as well as under inflammatory conditions. However, the atypical chemokine receptor CXCR7 is a rather neglected binding partner of CXCL12 although it binds to this chemokine with a 10-times stronger affinity than it's well-known receptor CXCR4. Additionally, CXCR7 can be engaged by another chemokine, CXCL11. In contrast to the conventional chemokine receptors which induce migration of cells, the engagement of the CXCR7 atypical chemokine receptor can result in cell migration, proliferation, survival or adhesion depending on the context of receptor engagement.
Physiologically, CXCR7 has been shown to be involved in heart formation and tissue remodelling. Additionally, CXCR7 has been implemented in various conditions such as rheumatic diseases or cancer and it appears to be a critical receptor driving tissue fibrosis. The clinical potential of targeting CXCR7 has been recognised more and more in the recent years and has been a target of several clinical drug developments. However, there are still many open questions and unknowns around the physiological and pathological functions of CXCR7.
Our lab has developed a loxP/cre model that allows for selective deletion of the CXCR7 gene to knockout CXCR7 in chosen cell types. Using this model we are investigating the role of CXCR7 in fibrosis . This is a project that lends itself to research opportunities for an Honours, Masters or PhD student.
This research project is available to PhD, Masters, Honours students to join as part of their thesis.
Please contact the Research Group Leader to discuss your options.
Sierro, F. et al. Disrupted cardiac development but normal hematopoiesis in mice deficient in the second CXCL12/SDF-1 receptor, CXCR7. Proc Natl Acad Sci USA 2007; 104: 14759-14764, doi:10.1073/pnas.0702229104.
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For further information about this research, please contact the research group leader.