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The role of complement properdin in bone biology


About This PhD Project

Project Description

Bone mineral density is routinely measured in those at risk of developing osteoporosis and in those on various treatments, and informs the management of a growing proportion of the population. A range of hormones, cytokines and environmental factors such as diet and exercise regulate bone mass and microarchitecture. Importantly, these can be measured reliably by micro-CT analysis of vertebrae prepared from mice. This method has revealed a significant difference between properdin deficient and wildtype mice at advanced age, which this project will characterise further.

We have previously shown that complement properdin shapes cellular responses, in particular of the macrophage lineage, to which osteoclasts belong. Osteoclasts and osteoblasts are the key bone matrix degrading and building cells, respectively, which we are able to differentiate from mouse bone marrow in vitro.

The project follows the hypothesis that there is an inherent difference in the cells with catabolic effect (osteoclasts) between properdin deficient and wildtype mice. Systemic factors relevant to bone biology will be measured. Aged male and female mice will be compared. The project will aid our understanding of bone biology in a novel area recently identified by the research group and will offer additional candidates to consider in treatment approaches, which aim to decrease fragility fractures.

References

Appelman-Dijkstra N, Papapoulos S. Novel approaches to the treatment of osteoporosis. Best Practice & Res Clin Endocr &Metab 2014; 28: 843-857.

Dupont A, Mohamed F, Salehen N, (…), Stover C. Septicaemia models using Streptococcus pneumoniae and Listeria monocytogenes: understanding the role of complement properdin. Med Microbiol Immunol. 2014;203:257-71

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