Journal article
Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice mice
EC Walker, NE McGregor, IJ Poulton, M Solano, S Pompolo, TJ Fernandes, MJ Constable, GC Nicholson, JG Zhang, NA Nicola, MT Gillespie, T John Martin, NA Sims
Journal of Clinical Investigation | AMER SOC CLINICAL INVESTIGATION INC | Published : 2010
DOI: 10.1172/JCI40568
Abstract
Effective osteoporosis therapy requires agents that increase the amount and/or quality of bone. Any modification of osteoclast-mediated bone resorption by disease or drug treatment, however, elicits a parallel change in osteoblast-mediated bone formation because the processes are tightly coupled. Anabolic approaches now focus on uncoupling osteoblast action from osteoclast formation, for example, by inhibiting sclerostin, an inhibitor of bone formation that does not influence osteoclast differentiation. Here, we report that oncostatin M (OSM) is produced by osteoblasts and osteocytes in mouse bone and that it has distinct effects when acting through 2 different receptors, OSM receptor (OSMR)..
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Awarded by National Health and Medical Research Council (NHMRC) (Australia)
Funding Acknowledgements
We thank John Wark and Susan Kantor at the Department of Medicine, Royal Melbourne Hospital, for use of their pQCT; Atsushi Miyajima, Tokyo University, and Anne Reutens, Monash University for Osmr<SUP>-/-</SUP> mice; and Gerard Karsenty, Columbia University, for the 6xOSE2 construct. We also thank staff at the Bioresources Centre, St. Vincent's Health, for excellent animal care. The work was supported by National Health and Medical Research Council (NHMRC) (Australia) program grants 345401 (to N.A. Sims, M.T. Gillespie, and T.J. Martin) and 461219 (to N.A. Nicola and J.G. Zhang). N.A. Sims is supported by a NHMRC (Australia) Senior Research Fellowship.