DICKKOPF-1 IS A MASTER REGULATOR OF JOINT REMODELING PDF

Degenerative and inflammatory joint diseases lead to a destruction of the joint architecture. Whereas degenerative osteoarthritis results in the formation of new bone, rheumatoid arthritis leads to bone resorption. The molecular basis of these different patterns of joint disease is unknown. By inhibiting Dickkopf-1 DKK-1 , a regulatory molecule of the Wnt pathway, we were able to reverse the bone-destructive pattern of a mouse model of rheumatoid arthritis to the bone-forming pattern of osteoarthritis. In this way, no overall bone erosion resulted, although bony nodules, so-called osteophytes, did form.

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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer.

In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. A Nature Research Journal. Degenerative and inflammatory joint diseases lead to a destruction of the joint architecture. Whereas degenerative osteoarthritis results in the formation of new bone, rheumatoid arthritis leads to bone resorption. The molecular basis of these different patterns of joint disease is unknown.

By inhibiting Dickkopf-1 DKK-1 , a regulatory molecule of the Wnt pathway, we were able to reverse the bone-destructive pattern of a mouse model of rheumatoid arthritis to the bone-forming pattern of osteoarthritis. In this way, no overall bone erosion resulted, although bony nodules, so-called osteophytes, did form. These results suggest that the Wnt pathway is a key regulator of joint remodeling. Firestein, G. Evolving concepts of rheumatoid arthritis.

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Keffer, J. Transgenic mice expressing human tumour necrosis factor: a predictive genetic model of arthritis. EMBO J. Gravallese, E. Identification of cell types responsible for bone resorption in rheumatoid arthritis and juvenile rheumatoid arthritis. Kong, Y. Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand. Pettit, A. Redlich, K. Osteoclasts are essential for TNF-alpha-mediated joint destruction. Miller, J.

The Wnts. Genome Biol. Mao, B. Holmen, S. Bone Miner. Glinka, A. Dickkopf-1 is a member of a new family of secreted proteins and functions in head induction. Bafico, A. Cell Biol. Morvan, F. Deletion of a single allele of the Dkk1 gene leads to an increase in bone formation and bone mass. Tian, E. The role of the Wnt-signaling antagonist DKK1 in the development of osteolytic lesions in multiple myeloma.

Van Beuningen, H. Osteoarthritis-like changes in the murine knee joint resulting from intra-articular transforming growth factor-beta injections. Osteoarthritis Cartilage 8 , 25—33 Scharstuhl, A. Adenoviral overexpression of Smad-7 and Smad-6 differentially regulates TGF-beta-mediated chondrocyte proliferation and proteoglycan synthesis.

Arthritis Rheum. Peifer, M. Wnt signaling in oncogenesis and embryogenesis—a look outside the nucleus. Science , — Lustig, B. Glass, D. II et al. Canonical Wnt signaling in differentiated osteoblasts controls osteoclast differentiation. Cell 8 , — Gong, Y. Cell , — Zwerina, J. Single and combined inhibition of tumor necrosis factor, interleukin-1, and RANKL pathways in tumor necrosis factor-induced arthritis: effects on synovial inflammation, bone erosion, and cartilage destruction.

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Garrett, S. A new approach to defining disease status in ankylosing spondylitis: the Bath Ankylosing Spondylitis Disease Activity Index. Gortz, B. Arthritis induces lymphocytic bone marrow inflammation and endosteal bone formation. Download references.

We thank E. Wagner for scientific discussions and B. Tuerk and M. Tryniecki for technical assistance. We also thank G. Wanivenhaus Medical University of Vienna for human synovial tissue samples and C. Hartmann Institute of Molecular Pathology for the osteocalcin probe.

Diarra conducted the in vivo analyses of hTNFtg mice and contributed to manuscript preparation. Dwyer conducted the analyses on collagen-induced arthritis. Reprints and Permissions. Diarra, D. Dickkopf-1 is a master regulator of joint remodeling.

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Dickkopf-1 Is a Master Regulator of Joint Remodeling

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. A Nature Research Journal. Degenerative and inflammatory joint diseases lead to a destruction of the joint architecture. Whereas degenerative osteoarthritis results in the formation of new bone, rheumatoid arthritis leads to bone resorption.

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Dickkopf-1 is a master regulator of joint remodeling

Skip to search form Skip to main content You are currently offline. Some features of the site may not work correctly. DOI: Degenerative and inflammatory joint diseases lead to a destruction of the joint architecture.

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Dickkopf-1 is a master regulator of joint remodeling.

What is this page? Degenerative and inflammatory joint diseases lead to a destruction of the joint architecture. Whereas degenerative osteoarthritis results in the formation of new bone, rheumatoid arthritis leads to bone resorption. The molecular basis of these different patterns of joint disease is unknown. By inhibiting Dickkopf-1 DKK-1 , a regulatory molecule of the Wnt pathway, we were able to reverse the bone-destructive pattern of a mouse model of rheumatoid arthritis to the bone-forming pattern of osteoarthritis. In this way, no overall bone erosion resulted, although bony nodules, so-called osteophytes, did form. We identified tumor necrosis factor-alpha TNF as a key inducer of DKK-1 in the mouse inflammatory arthritis model and in human rheumatoid arthritis.

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