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D1 Brunhilde Wirth, Anja Niehoff

Unravelling of novel pathomechanisms for bone and cartilage diseases

Prof. Dr. Brunhilde Wirth

Institute of Human Genetics
Faculty of Medicine, University of Cologne
Kerpener Str. 34, 50931 Cologne

 

PD Dr. Anja Niehoff

Cologne Center for Musculoskeletal Biomechanics (CCMB)
Faculty of Medicine, University of Cologne
Joseph-Stelzmann-Str. 9, 50931 Cologne

Institute of Biomechanics and Orthopaedics
German Sport University Cologne
Am Sportpark Müngersdorf 6, 50933 Cologne

Summary

The extracellular matrix (ECM) is connected via cell surface integrins to the actin cytoskeleton of the cell. Thereby, crucial chemical and mechanical signals for tissue morphogenesis, differentiation and homeostasis are transmitted. Plastin 3 (PLS3) is a ubiquitously present actin-binding and -bundling protein that regulates the dynamics of the actin cytoskeleton. Variants in PLS3 cause osteoporosis with fractures and PLS3 overexpression (OE) is a female protective modifier of spinal muscular atrophy (SMA).

Recently, it has been shown that PLS3 expression is associated with ECM degeneration in osteoarthritis. However, the exact function of PLS3 for ECM homeostasis in bone and cartilage is still unknown.

In our project we want to clarify the role of PLS3 in the pathogenesis of osteoporosis and osteoarthritis. To this end, we generated a conditional PLS3 OE mouse model and purchased a conditional Pls3 knockout (KO) mouse, generated by EUCOMM. Our results will be of highest relevance to develop future therapeutic approaches for these common diseases.