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3. List of Contributors

Author

Ackert-Bicknell, Cheryl, primary, Agarwal, Sunita K., additional, Albagha, Omar M.E., additional, Allen, Robyn S., additional, Arnold, Andrew, additional, Bassett, J.H. Duncan, additional, Bateman, John F., additional, Bellido, Teresita, additional, Bonewald, Lynda, additional, Boudin, Eveline, additional, Bouxsein, Mary L., additional, Boyce, Brendan F., additional, Brewer, Niambi S., additional, Brewster, Stephanie J., additional, Briggs, Mike, additional, Brown, Edward M., additional, Brown, Matthew A., additional, Bushinsky, David A., additional, Cabral, Wayne A., additional, Collins, Michael T., additional, Convente, Michael R., additional, Costa-Guda, Jessica, additional, Deng, Hong-Wen, additional, Devuyst, Olivier, additional, Drezner, Marc K., additional, Duncan, Emma L., additional, Egbuna, Ogo I., additional, Eisman, John A., additional, Farber, Charles R., additional, Feldman, David, additional, Ferreira, Carlos R., additional, Gahl, William A., additional, Gorvin, Caroline M., additional, Grol, Matthew W., additional, Guo, Yan, additional, Guse, Kilian, additional, Hannan, Fadil M., additional, Hao, Ruo-Han, additional, Holm, Ingrid A., additional, Igarashi, Takashi, additional, Jacobsen, Christina, additional, Johannesdottir, Fjola, additional, Jüppner, Harald, additional, Kaplan, Frederick S., additional, Karsenty, Gerard, additional, Kovacs, Christopher S., additional, Kuiper, John J., additional, Lee, Brendan H., additional, Loots, Gabriela G., additional, Lories, Rik J., additional, Luyten, Frank P., additional, Malloy, Peter J., additional, Mannstadt, Michael, additional, Marini, Joan C., additional, John Martin, T., additional, Miller, Walter L., additional, Moe, Orson W., additional, Newey, Paul J., additional, Nguyen, Tuan V., additional, Okamoto, Kazuo, additional, Pajevic, Paola D., additional, Papasian, Christopher J., additional, Piret, Siân E., additional, Ralston, Stuart H., additional, Rivadeneira, Fernando, additional, Robey, Pamela G., additional, Rosen, Clifford J., additional, Ruan, Merry Z.C., additional, Scheinman, Steven J., additional, Schurman, Scott J., additional, Sebastian, Aimy, additional, Shen, Yiping, additional, Shore, Eileen M., additional, Silve, Caroline, additional, Sims, Natalie A., additional, Stanley, Alexandra K., additional, Stone, Adrianne, additional, Takayanagi, Hiroshi, additional, Thakker, Rajesh V., additional, Towler, O. Will, additional, Uitterlinden, André G., additional, Valdes, Ana M., additional, van der Eerden, Bram C.J., additional, Van Hul, Wim, additional, Wei, Jianwen, additional, Wein, Marc N., additional, Weinstein, Lee S., additional, Whyte, Michael P., additional, Williams, Graham R., additional, Xing, Lianping, additional, Yang, Tie-Lin, additional, Zankl, Andreas, additional, Ziegler, Shira G., additional, and Zuscik, Michael J., additional

Published
2018
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8. List of Contributors

Author

Albagha, Omar M.E., primary, Arnold, Andrew, additional, Baldock, Paul, additional, Bouxsein, Mary L., additional, Boyce, Brendan F., additional, Brewster, Stephanie Jo, additional, Brown, Edward M., additional, Brown, Matthew A., additional, Bushinsky, David A., additional, Chakkalakal, Salin A., additional, Clifton-Bligh, Roderick, additional, Cole, William G., additional, Collins, Michael T., additional, Convente, Michael R., additional, Costa-Guda, Jessica, additional, Culbert, Andria L., additional, Deng, Hong-Wen, additional, Devuyst, Olivier, additional, Drezner, Marc K., additional, Duncan, Emma L., additional, Egbuna, Ogo I., additional, Eisman, John A., additional, Feldman, David, additional, Ferron, Mathieu, additional, Gild, Matti, additional, Guo, Yan, additional, Guse, Kilian, additional, Holm, Ingrid A., additional, Hudson, Bryan, additional, Igarashi, Takashi, additional, Jacobsen, Christina, additional, Jüppner, Harald, additional, Kaplan, Frederick S., additional, Karsenty, Gerard, additional, Kovacs, Christopher S., additional, Lee, Brendan, additional, Loots, Gabriela G., additional, Lories, Rik J., additional, Lounev, Vitali Y., additional, Luyten, Frank P., additional, Malloy, Peter J., additional, Marini, Joan C., additional, John Martin, T., additional, Miller, Walter L., additional, Moe, Orson W., additional, Nguyen, Tuan V., additional, Oury, Franck, additional, Papasian, Christopher J., additional, Patel, Dhruval, additional, Perdu, Bram, additional, Piret, Siân E., additional, Helen Rajpar, M., additional, Ralston, Stuart H, additional, Rivadeneira, Fernando, additional, Robinson, Bruce G, additional, Ruan, Merry ZC, additional, Scheinman, Steven J., additional, Schurman, Scott J., additional, Shen, Yiping, additional, Shore, Eileen M., additional, Silve, Caroline, additional, Sims, Natalie A., additional, Singh, Anil, additional, Spiegel, Allen M., additional, Thakker, Rajesh V., additional, Uitterlinden, André G., additional, Valdes, Ana M., additional, Van Hul, Wim, additional, Weinstein, Lee S., additional, Whyte, Michael P., additional, Xing, Lianping, additional, Yang, Tie-Lin, additional, and Zuscik, Michael J., additional

Published
2013
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14. In Memoriam: Stephen M Krane

Author

Dayer, Jean-Michel, primary, Goldring, Mary B, additional, Goldring, Steven R, additional, Kronenberg, Henry M, additional, John Martin, T, additional, and Graham G Russell, R, additional

Published
2015
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16. Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice mice.

Author

Poulton I.J., McGregor N.E., Walker E.C., Sims N.A., John Martin T., Gillespie M.T., Nicola N.A., Zhang J.-G., Nicholson G.C., Constable M.J., Fernandes T.J., Pompolo S., Solano M., Poulton I.J., McGregor N.E., Walker E.C., Sims N.A., John Martin T., Gillespie M.T., Nicola N.A., Zhang J.-G., Nicholson G.C., Constable M.J., Fernandes T.J., Pompolo S., and Solano M.

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) and leukemia inhibitory factor receptor (LIFR). Specifically, mouse OSM (mOSM) inhibited sclerostin production in a stromal cell line and in primary murine osteoblast cultures by acting through LIFR. In contrast, when acting through OSMR, mOSM stimulated RANKL production and osteoclast formation. A key role for OSMR in bone turnover was confirmed by the osteopetrotic phenotype of mice lacking OSMR. Furthermore, in contrast to the accepted model, in which mOSM acts only through OSMR, mOSM inhibited sclerostin expression in Osmr-/- osteoblasts and enhanced bone formation in vivo. These data reveal what we believe to be a novel pathway by which bone formation can be stimulated independently of bone resorption and provide new insights into OSMR and LIFR signaling that are relevant to other medical conditions, including cardiovascular and neurodegenerative diseases and cancer.

Published
2012

17. Model structure and control of bone remodeling: A theoretical study

Author

Pivonka, P., Zimak, J., Smith, D.W., Gardiner, B.S., Dunstan, C.R., Sims, N.A., John Martin, T., Mundy, G.R., Pivonka, P., Zimak, J., Smith, D.W., Gardiner, B.S., Dunstan, C.R., Sims, N.A., John Martin, T., and Mundy, G.R.

Abstract

It is generally accepted that RANKL is highly expressed in osteoblast precursor cells while OPG is highly expressed in mature osteoblasts, but to date no functional utility to the BMU has been proposed for this particular ligand–decoy–receptor expression profile. As discovered in the mid 90s, the RANK–RANKL–OPG signaling cascade is a major signaling pathway regulating bone remodeling. In this paper we study theoretically the functional implications of particular RANKL/OPG expression profiles on bone volume. For this purpose we formulate an extended bone–cell dynamics model describing functional behaviour of basic multicellular units (BMUs) responsible for bone resorption and formation. This model incorporates the RANK–RANKL–OPG signaling together with the regulating action of TGF-β on bone cells. The bone–cell population model employed here builds on the work of Lemaire et al. (2004) [1], but incorporates the following significant modifications: (i) addition of a rate equation describing changes in bone volume with time as the key ‘output function’ tracking functional behaviour of BMUs, (ii) a rate equation describing release of TGF-β from the bone matrix, (iii) expression of OPG and RANKL on both osteoblastic cell lines, and (iv) modified activator/repressor functions. Using bone volume as a functional selection criterion, we find that there is a preferred arrangement for ligand expression on particular cell types, and further, that this arrangement coincides with biological observations. We then investigate the model parameter space combinatorially, searching for preferred ‘groupings’ of changes in differentiation rates of various cell types. Again, a criterion of bone volume change is employed to identify possible ways of optimally controlling BMU responses. While some combinations of changes in differentiation rates are clearly unrealistic, other combinations of changes in differentiation rates are potentially functionally significant. Most importantly, the comb

Published
2008

19. Parathyroid hormone-related protein production in the lamprey Geotria australis: developmental and evolutionary perspectives

Author

Trivett, M.K., Potter, I.C., Power, G., Zhou, H., Macmillan, D.L., John Martin, T., Danks, J.A., Trivett, M.K., Potter, I.C., Power, G., Zhou, H., Macmillan, D.L., John Martin, T., and Danks, J.A.

Abstract

This study explored the distribution of parathyroid hormone-related protein (PTHrP) and its mRNA in tissues of the lamprey Geotria australis, a representative of one of the two surviving groups of an early and jawless stage in vertebrate evolution. For this purpose, antibodies to N-terminal and mid-molecule human PTHrP were used to determine the locations of the antigen. Sites of mRNA production were demonstrated by in situ hybridisation with a digoxigenin-labelled riboprobe to exon VI of the human PTHrP gene. The results revealed that antigen and its mRNA were widely distributed among similar sites of tissue localisation to those described for mammalian and avian species. However, some novel sites of localisation, such as in the gill and notochord, were also found. Some differences in PTHrP localisation were noted among individuals at different intervals of the life cycle, indicating that the distributions of PTHrP, and possibly its roles, change with the stage of development in this species. The widespread tissue distribution in G. australis implies diverse physiological roles for this protein. The presence of PTHrP in the lamprey, a representative of a group of vertebrates, which apparently evolved over 540 million years ago, strongly suggests that it is a protein of ancient origin. In addition, the successful use of antibodies and probes based on the human sequence in the lamprey also provides evidence that the PTHrP molecule may have been conserved from lampreys through to humans.

Published
2005

21. Novel and selective small molecule stimulators of osteoprotegerin expression inhibit bone resorption.

Author

E, Onyia Jude, Sells, Galvin Rachelle J, L, Ma Yanfei, L, Halladay David, R, Miles Rebecca, Xuhao, Yang, Tina, Fuson, L, Cain Ricky, Qiang, Zeng Qing, S, Chandrasekhar, Renee, Emkey, Yanping, Xu, Kannan, Thirunavukkarasu, U, Bryant Henry, and John, Martin T

Abstract

Osteoprotegerin (OPG), a secreted member of the tumor necrosis factor receptor superfamily, is a potent inhibitor of osteoclast formation and bone resorption. Because OPG functions physiologically as a locally generated (paracrine) factor, we used high-throughput screening to identify small molecules that enhance the activity of the promoter of the human OPG gene. We found three structurally unrelated compounds that selectively increased OPG gene transcription, OPG mRNA levels, and OPG protein production and release by osteoblastic cells. Structural analysis of one compound, a benzamide derivative, led to the identification of four related molecules, which are also OPG inducers. The most potent of these compounds, Cmpd 5 inhibited osteoclast formation and parathyroid hormone-induced calvarial bone resorption. In vivo, Cmpd 5 completely blocked resorptive activity (serum calcium, osteoclast number) in parathyroid hormone-treated rats. Furthermore, Cmpd 5 reduced the ability of a rat breast cancer to metastasize to bone. Finally, the compound also prevented bone loss in a rat adjuvant arthritis model. These results provide proof of the concept that low molecular weight compounds can enhance OPG production in ways that can result in effective therapies.

Published
2004

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