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Lookup NU author(s): Dr Philip Dobson, Dr Mariana Rocha, Dr John Grady, Alexia Chrysostomou, Sharon Watson, Professor Laura GreavesORCiD, Professor David Deehan, Emeritus Professor Doug Turnbull
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Fragility fractures caused by osteoporosis affect millions of people worldwide every year with significant levels of associated morbidity, mortality and costs to the healthcare economy. The pathogenesis of declining bone mineral density is poorly understood but it is inherently related to increasing age. Growing evidence in recent years, especially that provided by mouse models, suggest that accumulating somatic mitochondrial DNA mutations may cause the phenotypic changes associated with the ageing process including osteoporosis. Methods to study mitochondrial abnormalities in individual osteoblasts, osteoclasts and osteocytes are limited and impair our ability to assess the changes seen with age and in animal models of ageing. To enable the assessment of mitochondrial protein levels, we have developed a quadruple immunofluorescence method to accurately quantify the presence of mitochondrial respiratory chain components within individual bone cells. We have applied this technique to a well-established mouse model of ageing and osteoporosis and show respiratory chain deficiency.
Author(s): Dobson PF, Rocha MC, Grady JP, Chrysostomou A, Hipps D, Watson S, Greaves LC, Deehan DJ, Turnbull DM
Publication type: Article
Publication status: Published
Journal: Scientific Reports
Year: 2016
Volume: 6
Online publication date: 24/08/2016
Acceptance date: 06/07/2016
Date deposited: 18/10/2016
ISSN (electronic): 2045-2322
Publisher: Nature Publishing Group
URL: http://dx.doi.org/10.1038/srep31907
DOI: 10.1038/srep31907
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