Vision: To determine the mechanisms underpinning how cell-matrix interactions control normal tissue formation and function, and how their disruption causes disease.
This year as part of the British Science Week celebrations, the Centre along with colleagues from across FBMH took over Manchester Museum for the Body Experience. With people waiting for the doors to open at 10am, the visitors were non-stop! The Thornton, Lennon, Streuli, Gilmore and Swift labs worked incredibly hard entertaining and inspiring the public all day. We saw over 2000 visitors, handed out 750 passports and 500 bags, hosted over 80 researchers across 18 stands with 12 volunteers Read more
Press release: Yang, N., Williams, J., Pekovic-Vaughan, V., Wang, P., Olabi, S., McConnell, J., Gossan, N., Hughes, A., Cheung, J., Streuli, C.H.* and Meng, Q.-J.* (2017) Cellular mechano-environment regulates the mammary circadian clock. Nat Commun. 8, 14287. PubMed.*Joint senior/contributing authors. Read more
Shireen Lamandé, Murdoch Childrens Research Institute, Melbourne "Inherited musculoskeletal disorders: molecular genetics and cellular mechanisms." Our goal is to identify the genetic basis of inherited extracellular matrix disorders, to understand how mutations cause disease, and identify pathogenic pathways that can be manipulated pharmacologically. I will provide some snapshots of our recent work on TRPV4 and collagen disorders. Read more
Our studies showed that in human knee cartilage the expression of a core circadian clock protein BMAL1 was progressively decreased in diseased joints. To investigate what happens to cartilage when it is devoid of circadian rhythm we created a transgenic mouse with selective deletion of Bmal1 mainly in cartilage cells. The tissue-specific Bmal1 deletion led to profound degeneration of articular cartilage in the knees. Gene expression analysis of normal and mutant cartilage showed that many Read more
We have discovered that in addition to CCL5, CXCL8 and CXCL11, TSG-6 interacts with at least 7 other chemokines (i.e. CCL2, CCL7, CCL19, CCL21, CCL27, CXCL4, and CXCL12) including those involved in both homeostatic and inflammatory functions. TSG-6 interacts (via its Link module) with the GAG-binding site on the chemokines, thereby inhibiting the binding of chemokines to GAGs and their presentation on endothelial cells; TSG-6 also inhibits the binding of chemokines to collagen, providing another Read more