Clinical Investigation. Natalie Sims and colleagues from The University of Melbourne, Australia, resolve the effects of these signaling pathways by targeted mutagenesis of gp130 in mice, which rendered them deficient in either STAT1/3 activation or SHP2/ras/MAPK activation. The authors report that STAT1/3 activation is involved in the proliferation of chondrocytes and osteoblasts cells crucial to bone formation, whereas SHP2/ras/MAPK activation plays a key role in inhibiting osteoclasts cells causing bone breakdown. These insights may provide new therapeutic targets for improving bone growth and bone density in mammals.

TITLE: Glycoprotein 130 regulates bone turnover and bone size by distinct downstream signaling pathways

AUTHOR CONTACT:
Natalie A. Sims
The University of Melbourne, Fitzroy, Victoria, Australia.
Phone: 61-3-9288-2555
Fax: 61-3-9288-2581
E-mail: nsims@medstv.unimelb.edu.au

View the PDF of this article at: https://www.the-jci.org/press/19872.pdf

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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
2-Feb-2004

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