Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Schneider, M.R. et al.

Marlon R. Schneider, Bettina Mayer-Roenne, Maik Dahlhoff, Verena Proell, Karin Weber, Eckhard Wolf, Reinhold G. Erben,

High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.

Signaling through the epidermal growth factor receptor (EGFR) by ligands such as epidermal growth factor (EGF), transforming growth factor alpha (TGFA), and amphiregulin (AREG) has been reported to have effects on skeletal growth. The role of betacellulin (BTC), another EGFR ligand, in skeletal development and bone metabolism is unknown. In previous experiments, transgenic mice overexpressing BTC ubiquitously under the control of the chicken beta-actin promoter (BTC-tg) exhibited stunted growth and disproportionately sized long bones. In this study, we performed a detailed phenotypic analysis of BTC-tg mice at 3, 6, and 9 wk of age. Osteoblastic cells from transgenic mice showed strong expression of BTC as determined by Western blots and by immunohistochemistry on bone sections. In femurs of male and female BTC-tg mice, we found reduced longitudinal bone growth and a pronounced increase in total volumetric BMD. The increased femoral BMD was mainly caused by augmented endocortical bone apposition and subsequent cortical bone thickening. In contrast, vertebral BMD was reduced in BTC-tg mice of both sexes. An overall similar phenotype was found in 6-mo-old BTC-tg mice. The increase in cortical bone mass in the appendicular skeleton of BTC-tg mice was largely blocked when they were crossed into the Egfr (Wa5) background characterized by a dominant negative EGFR. Our study showed that overexpression of BTC results in an EGFR-dependent upregulation of cortical bone mass in the appendicular skeleton of mice, uncovering a potential novel anabolic pathway for cortical bone.[1]

References

High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent. Schneider, M.R., Mayer-Roenne, B., Dahlhoff, M., Proell, V., Weber, K., Wolf, E., Erben, R.G. J. Bone Miner. Res. (2009) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.