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Selenium pp 573-587 | Cite as

Selenoproteins in Skeletal Development and Disease: Lessons from Trsp Deletion in Murine Bone and Cartilage Progenitor Cells

Chapter

Abstract

The use of global gene disruption to study the roles of specific selenoproteins in skeletal development and homeostasis can be handicapped by the difficulty in determining whether or not any observed phenotype is attributable to losses of gene function specifically in chondrocytes, osteoblasts, or osteoclasts. Indeed, the potential effects of global gene knockouts on the brain, kidney, endocrine glands, and hematopoietic system, tissues involved in the regulating skeleton growth and ­function, can confound phenotypic analyses. Tissue-specific gene alterations, in contrast, have the ability to reveal information about selenoprotein gene function within cells directly involved in skeletal growth and homeostasis. The dramatic phenotype resulting from disruption of Trsp in osteo-chondroprogenitor cells, for example, illustrates how bone and cartilage development are critically dependent on normal selenoprotein function.

Keywords

Reactive Oxygen Species GPx4 Activity Epiphyseal Growth Plate Osteoblast Apoptosis Selenoprotein Gene 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Acknowledgements

The studies described herein were supported by grants from the Arthritis Society of Canada and the Alberta Cancer Board. CD held an Alberta Cancer Board studentship and FRJ was the recipient of a Canada Research Chairs award.

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Department of Biochemistry and Molecular Biology, The McCaig Institute for Bone and Joint HealthUniversity of CalgaryCalgaryCanada

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