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KMID : 0354619960080010049
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Journal Dankook Dental Research Institute
1996 Volume.8 No. 1 p.49 ~ p.58
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Effects of Interleukin-1 and Tumor Necrosis Factor- on the Nitric Oxide Production from Mouse Osteoblast in Culture
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Abstract
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Bone remodeling is characterized by the coupling of osteoclast-mediated bone resorption and osteoblast-mediated bone formation. The process is tightly regulated at the local level by an incompletely known complex network of humoral factors
produced
in
the bone microenvironment, including peptide as well as non-peptide molecules. Nitric oxide (NO) is recently identified messenger molecule regulating a wide range of functions throughout the body but little is known about its possible role in
skeletal
metabolism. Many other cells, including macrophages, hepatocytes, chondrocytes and bone marrow cells, also produce NO. Recently, NO was reported to inhibit osteoclastic bone resorption in vitro, and there are indications of an arginine-dependent
NO
pathway in osteoblasts and osteoclasts. In this study we present evidence that mouse osteoblasts can be induced to produce NO by cytokines (interleukin-1β(IL-1β), tumor necrosis factor-α (TNF-α) known tio modulate bone cell activity.
@ES The observed results were as follows.
@EN 1. In case of 24 hr incubation with IL-1β, NO production of MC3T3/E1 cells was not stimulated. But significant amounts of NO were measured after 48 hr incubation. In case of TNF-α, significant amounts of NO were measured after 24 hr, and
increased
further during the next 48 hr followed by a much slower increase up to 96 hrs.
2. IL-1β stimulated NO production into cultured medium in cultures of MC3T3/E1 cells dose dependently (0.2, 1, 1 ng/ml).
3. TNF-α stimulated NO production into cultured medium in cultures of MC3T3/E1 cells dose dependently (0.2, 1, 5 ng/ml).
4. Cytokine combination increased NO production dose dependently. And synergistic effects of the two cytokines were observed at all dose combinations.
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KEYWORD
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