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MeSH Review


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Disease relevance of Osteoclasts


High impact information on Osteoclasts

  • New insights into estrogen receptor structure and function, recent discoveries about the development and activity of osteoclasts, and lessons learned from human and animal genetic mutations have all contributed to increased understanding of the skeletal effects of estrogen, both in males and females [6].
  • TSH inhibits osteoclast formation and survival by attenuating JNK/c-jun and NFkappaB signaling triggered in response to RANK-L and TNFalpha [7].
  • In endochondral skeletal elements of Osx null mice, mesenchymal cells, together with osteoclasts and blood vessels, invade the mineralized cartilage matrix [8].
  • We conclude that ClC-7 provides the chloride conductance required for an efficient proton pumping by the H(+)-ATPase of the osteoclast ruffled membrane [9].
  • Fosl1 is a transcriptional target of c-Fos during osteoclast differentiation [10].

Chemical compound and disease context of Osteoclasts

  • These data suggest that the protective effects of estrogen against postmenopausal osteoporosis are mediated in part by the direct induction of apoptosis of the bone-resorbing osteoclasts by an estrogen receptor- mediated mechanism [11].
  • Inflammatory bone loss is accompanied by osteoclast formation induced by bone-resorbing cytokines, but the mechanism of PGE2 production and bone resorption in vivo is not fully understood [12].
  • ICI164,384 and tamoxifen, as pure and partial antagonists, respectively, completely or partially blocked the effect of E2 on both inhibition of osteoclastic bone resorption and induction of osteoclast apoptosis [11].
  • Alendronate inhibited bone resorption by isolated chicken or rat osteoclasts when the amount on the bone surface was around 1.3 x 10(-3) fmol/microns 2, which would produce a concentration of 0.1-1 mM in the resorption space if 50% were released [13].
  • In unstimulated cultures it appears that HU inhibits bone resorption by affecting mechanisms that are independent of changes in osteoclast number and that may be influenced by cell replication or other unknown factors [14].

Biological context of Osteoclasts


Anatomical context of Osteoclasts


Associations of Osteoclasts with chemical compounds

  • Moreover, we provide genetic and biochemical evidence for the role of Syk tyrosine kinase as a crucial upstream regulator of Vav3 in osteoclasts [17].
  • The association between PU.1 and osteoclast differentiation was confirmed by demonstrating that PU.1 expression increased with the induction of osteoclastogenesis by either 1,25-dihydroxyvitamin D3 or dexamethasone [23].
  • Cathepsin K, a cysteine protease gene that is highly expressed in osteoclasts, localized to the pycnodysostosis region [24].
  • The processes governing both the differentiation and activation of osteoclasts involve signals induced by osteoprotegerin ligand (OPGL), a member of tumor necrosis factor (TNF) superfamily, and its cognate receptor RANK [25].
  • Furthermore, an unphosphorylatable mutant at the MAPK consensus serine is specifically deficient in formation of multinucleated osteoclasts, mimicking the defect in Mitf(mi/mi) mice [26].

Gene context of Osteoclasts

  • Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation [20].
  • These data suggest that OPGL is an osteoclast differentiation and activation factor [20].
  • However, the specific signalling pathways that require c-Src expression for normal osteoclast activity have not been elucidated [16].
  • Among NFAT proteins, NFATc1 is crucial for the differentiation of bone-resorbing osteoclasts [27].
  • Vav3 regulates osteoclast function and bone mass [17].

Analytical, diagnostic and therapeutic context of Osteoclasts


  1. Use of dichloromethylene diphosphonate in metastatic bone disease. Jung, A., Chantraine, A., Donath, A., van Ouwenaller, C., Turnill, D., Mermillod, B., Kitler, M.E. N. Engl. J. Med. (1983) [Pubmed]
  2. Selective inhibition of NF-kappa B blocks osteoclastogenesis and prevents inflammatory bone destruction in vivo. Jimi, E., Aoki, K., Saito, H., D'Acquisto, F., May, M.J., Nakamura, I., Sudo, T., Kojima, T., Okamoto, F., Fukushima, H., Okabe, K., Ohya, K., Ghosh, S. Nat. Med. (2004) [Pubmed]
  3. Osteopetrosis in mice lacking NF-kappaB1 and NF-kappaB2. Iotsova, V., Caamaño, J., Loy, J., Yang, Y., Lewin, A., Bravo, R. Nat. Med. (1997) [Pubmed]
  4. Osteoprotegerin blocks bone cancer-induced skeletal destruction, skeletal pain and pain-related neurochemical reorganization of the spinal cord. Honore, P., Luger, N.M., Sabino, M.A., Schwei, M.J., Rogers, S.D., Mach, D.B., O'keefe, P.F., Ramnaraine, M.L., Clohisy, D.R., Mantyh, P.W. Nat. Med. (2000) [Pubmed]
  5. Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families. Suda, T., Takahashi, N., Udagawa, N., Jimi, E., Gillespie, M.T., Martin, T.J. Endocr. Rev. (1999) [Pubmed]
  6. Sex steroids and bone. Compston, J.E. Physiol. Rev. (2001) [Pubmed]
  7. TSH is a negative regulator of skeletal remodeling. Abe, E., Marians, R.C., Yu, W., Wu, X.B., Ando, T., Li, Y., Iqbal, J., Eldeiry, L., Rajendren, G., Blair, H.C., Davies, T.F., Zaidi, M. Cell (2003) [Pubmed]
  8. The novel zinc finger-containing transcription factor osterix is required for osteoblast differentiation and bone formation. Nakashima, K., Zhou, X., Kunkel, G., Zhang, Z., Deng, J.M., Behringer, R.R., de Crombrugghe, B. Cell (2002) [Pubmed]
  9. Loss of the ClC-7 chloride channel leads to osteopetrosis in mice and man. Kornak, U., Kasper, D., Bösl, M.R., Kaiser, E., Schweizer, M., Schulz, A., Friedrich, W., Delling, G., Jentsch, T.J. Cell (2001) [Pubmed]
  10. Fosl1 is a transcriptional target of c-Fos during osteoclast differentiation. Matsuo, K., Owens, J.M., Tonko, M., Elliott, C., Chambers, T.J., Wagner, E.F. Nat. Genet. (2000) [Pubmed]
  11. Estrogen inhibits bone resorption by directly inducing apoptosis of the bone-resorbing osteoclasts. Kameda, T., Mano, H., Yuasa, T., Mori, Y., Miyazawa, K., Shiokawa, M., Nakamaru, Y., Hiroi, E., Hiura, K., Kameda, A., Yang, N.N., Hakeda, Y., Kumegawa, M. J. Exp. Med. (1997) [Pubmed]
  12. An essential role of cytosolic phospholipase A2alpha in prostaglandin E2-mediated bone resorption associated with inflammation. Miyaura, C., Inada, M., Matsumoto, C., Ohshiba, T., Uozumi, N., Shimizu, T., Ito, A. J. Exp. Med. (2003) [Pubmed]
  13. Bisphosphonate action. Alendronate localization in rat bone and effects on osteoclast ultrastructure. Sato, M., Grasser, W., Endo, N., Akins, R., Simmons, H., Thompson, D.D., Golub, E., Rodan, G.A. J. Clin. Invest. (1991) [Pubmed]
  14. DNA synthesis is not necessary for osteoclastic responses to parathyroid hormone in cultured fetal rat long bones. Lorenzo, J.A., Raisz, L.G., Hock, J.M. J. Clin. Invest. (1983) [Pubmed]
  15. Estrogen promotes apoptosis of murine osteoclasts mediated by TGF-beta. Hughes, D.E., Dai, A., Tiffee, J.C., Li, H.H., Mundy, G.R., Boyce, B.F. Nat. Med. (1996) [Pubmed]
  16. c-Cbl is downstream of c-Src in a signalling pathway necessary for bone resorption. Tanaka, S., Amling, M., Neff, L., Peyman, A., Uhlmann, E., Levy, J.B., Baron, R. Nature (1996) [Pubmed]
  17. Vav3 regulates osteoclast function and bone mass. Faccio, R., Teitelbaum, S.L., Fujikawa, K., Chappel, J., Zallone, A., Tybulewicz, V.L., Ross, F.P., Swat, W. Nat. Med. (2005) [Pubmed]
  18. RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-beta. Takayanagi, H., Kim, S., Matsuo, K., Suzuki, H., Suzuki, T., Sato, K., Yokochi, T., Oda, H., Nakamura, K., Ida, N., Wagner, E.F., Taniguchi, T. Nature (2002) [Pubmed]
  19. Enforced expression of Bcl-2 in monocytes rescues macrophages and partially reverses osteopetrosis in op/op mice. Lagasse, E., Weissman, I.L. Cell (1997) [Pubmed]
  20. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Lacey, D.L., Timms, E., Tan, H.L., Kelley, M.J., Dunstan, C.R., Burgess, T., Elliott, R., Colombero, A., Elliott, G., Scully, S., Hsu, H., Sullivan, J., Hawkins, N., Davy, E., Capparelli, C., Eli, A., Qian, Y.X., Kaufman, S., Sarosi, I., Shalhoub, V., Senaldi, G., Guo, J., Delaney, J., Boyle, W.J. Cell (1998) [Pubmed]
  21. Commitment to the B-lymphoid lineage depends on the transcription factor Pax5. Nutt, S.L., Heavey, B., Rolink, A.G., Busslinger, M. Nature (1999) [Pubmed]
  22. Growth hormone and bone. Ohlsson, C., Bengtsson, B.A., Isaksson, O.G., Andreassen, T.T., Slootweg, M.C. Endocr. Rev. (1998) [Pubmed]
  23. Osteopetrosis in mice lacking haematopoietic transcription factor PU.1. Tondravi, M.M., McKercher, S.R., Anderson, K., Erdmann, J.M., Quiroz, M., Maki, R., Teitelbaum, S.L. Nature (1997) [Pubmed]
  24. Pycnodysostosis, a lysosomal disease caused by cathepsin K deficiency. Gelb, B.D., Shi, G.P., Chapman, H.A., Desnick, R.J. Science (1996) [Pubmed]
  25. TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling. Lomaga, M.A., Yeh, W.C., Sarosi, I., Duncan, G.S., Furlonger, C., Ho, A., Morony, S., Capparelli, C., Van, G., Kaufman, S., van der Heiden, A., Itie, A., Wakeham, A., Khoo, W., Sasaki, T., Cao, Z., Penninger, J.M., Paige, C.J., Lacey, D.L., Dunstan, C.R., Boyle, W.J., Goeddel, D.V., Mak, T.W. Genes Dev. (1999) [Pubmed]
  26. Linkage of M-CSF signaling to Mitf, TFE3, and the osteoclast defect in Mitf(mi/mi) mice. Weilbaecher, K.N., Motyckova, G., Huber, W.E., Takemoto, C.M., Hemesath, T.J., Xu, Y., Hershey, C.L., Dowland, N.R., Wells, A.G., Fisher, D.E. Mol. Cell (2001) [Pubmed]
  27. NFAT and Osterix cooperatively regulate bone formation. Koga, T., Matsui, Y., Asagiri, M., Kodama, T., de Crombrugghe, B., Nakashima, K., Takayanagi, H. Nat. Med. (2005) [Pubmed]
  28. Increased osteoclast development after estrogen loss: mediation by interleukin-6. Jilka, R.L., Hangoc, G., Girasole, G., Passeri, G., Williams, D.C., Abrams, J.S., Boyce, B., Broxmeyer, H., Manolagas, S.C. Science (1992) [Pubmed]
  29. Interleukin (IL)-6 induction of osteoclast differentiation depends on IL-6 receptors expressed on osteoblastic cells but not on osteoclast progenitors. Udagawa, N., Takahashi, N., Katagiri, T., Tamura, T., Wada, S., Findlay, D.M., Martin, T.J., Hirota, H., Taga, T., Kishimoto, T., Suda, T. J. Exp. Med. (1995) [Pubmed]
  30. IL-1 receptor-associated kinase M is a central regulator of osteoclast differentiation and activation. Li, H., Cuartas, E., Cui, W., Choi, Y., Crawford, T.D., Ke, H.Z., Kobayashi, K.S., Flavell, R.A., Vignery, A. J. Exp. Med. (2005) [Pubmed]
  31. Echistatin is a potent inhibitor of bone resorption in culture. Sato, M., Sardana, M.K., Grasser, W.A., Garsky, V.M., Murray, J.M., Gould, R.J. J. Cell Biol. (1990) [Pubmed]
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