Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by KUROKI, T.
Right arrow Articles by NOBUNAGA, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by KUROKI, T.
Right arrow Articles by NOBUNAGA, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1994 British Society for Rheumatology

research-article

EFFECTS OF CYTOKINES ON ALKALINE PHOSPHATASE AND OSTEOCALCIN PRODUCTION, CALCIFICATION AND CALCIUM RELEASE BY HUMAN OSTEOBLASTIC CELLS

T. KUROKI*, M. SHINGU*, Y. KOSHIHARA{dagger} and M. NOBUNAGA*

*Department of Clinical Immunology, Medical Institute of Bioregulation, Kyushu University 69 Tsurumihara, Beppu, Japan 874
{dagger}Department of Biosignal Research, Tokyo Metropolitan Institute of Gerontology 35-2, Sakaecho, Itabashiku, Tokyo, Japan 173

Correspondence to: M. Shingu

We examined the effect of TNF-{alpha}, IL-1ß and IL-6 on alkaline phosphatase (ALP) and osteocalcin (OC) production, calcification and calcium (Ca) release in human osteoblastic cell cultures obtained from human periosteum. The cells were cultured with varying concentrations of cytokines for 3 days. TNF-{alpha} and IL-1ß significantly inhibited ALP production, decreased cellular Ca content, and significantly enhanced 45Ca release in human osteoblastic cells. IL-6, on the other hand, significantly suppressed 45Ca release by osteoblastic cells. These cytokines did not influence the production of OC by osteoblastic cells. The results obtained suggest that TNF-{alpha} and IL-1ß may inhibit bone formation and calcification and that the effects of IL-6 on osteoblastic cells may be different from those of TNF-{alpha} or IL-1ß. These effects on osteoblastic cells may be one of the mechanisms by which bone loss occurs in patients with RA.

KEY WORDS: Cytokine, Human osteoblastic cells, Calcification, Calcium release


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
K. Redlich, B. Gortz, S. Hayer, J. Zwerina, N. Doerr, P. Kostenuik, H. Bergmeister, G. Kollias, G. Steiner, J. S. Smolen, et al.
Repair of Local Bone Erosions and Reversal of Systemic Bone Loss Upon Therapy with Anti-Tumor Necrosis Factor in Combination with Osteoprotegerin or Parathyroid Hormone in Tumor Necrosis Factor-Mediated Arthritis
Am. J. Pathol., February 1, 2004; 164(2): 543 - 555.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
L. Gilbert, X. He, P. Farmer, S. Boden, M. Kozlowski, J. Rubin, and M. S. Nanes
Inhibition of Osteoblast Differentiation by Tumor Necrosis Factor-{alpha}
Endocrinology, November 1, 2000; 141(11): 3956 - 3964.
[Abstract] [Full Text] [PDF]

Home page
 Rheumatology (Oxford)Home page
P. Oelzner, S. Franke, A. Muller, G. Hein, and G. Stein
Relationship between soluble markers of immune activation and bone turnover in post-menopausal women with rheumatoid arthritis
Rheumatology, September 1, 1999; 38(9): 841 - 847.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
S. Agarwal, C. S. Chandra, N. P. Piesco, H. H. Langkamp, L. Bowen, and C. Baran
Regulation of Periodontal Ligament Cell Functions by Interleukin-1beta
Infect. Immun., March 1, 1998; 66(3): 932 - 937.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.