• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.39-47
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• 2007

Bone undergoes continuous remodeling throughout the life and bone health is governed by the balance of bone resorbing osteoclast and bone forming osteoblast. Bone resorption is reflected in tartrate resistant acid phosphatase, pyridinium cross link and collagen telopeptide, whereas bone formation activity can be expressed as bone specific alkaline phosphatase, osteocalcin and procollagen I extension peptide. Milk basic protein and lactoferrin have been reported as active proteins to modulating bone metabolism. In addition to these proteins, some bioactive milk peptides released during lactic fermentation may provide beneficial effect on bone metabolism. The effects of fermented products of Lactobacillus casei ATCC 393 on bone metabolism were investigated using a variety of biochemical markers in osteoblastic MC3T3-E1 cells and ovariectomized rats. Based on the results, the fermented products of Lactobacillus casei ATCC 393 played an functional role in bone metabolism by suppressing bone resorption and by increasing bone formation.

• International Journal of Oral Biology
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• v.36 no.4
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• pp.173-178
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• 2011

Tumor necrosis factor alpha ($TNF{\alpha}$) is a multifunctional cytokine that is elevated in inflammatory diseases such as atherosclerosis, diabetes and rheumatoid arthritis. Recent evidence has suggested that ${\beta}2$ adrenergic receptor (${\beta}2AR$) activation in osteoblasts suppresses osteogenic activity. In the present study, we explored whether $TNF{\alpha}$ modulates ${\beta}AR$ expression in osteoblastic cells and whether this regulation is associated with the inhibition of osteoblast differentiation by $TNF{\alpha}$. In the experiments, we used C2C12 cells, MC3T3-E1 cells and primary cultured mouse bone marrow stromal cells. Among the three subtypes of ${\beta}AR$, ${\beta}2$ and ${\beta}3AR$ were found in our analysis to be upregulated by $TNF{\alpha}$. Moreover, isoproterenol-induced cAMP production was observed to be significantly enhanced in $TNF{\alpha}$-primed C2C12 cells, indicating that $TNF{\alpha}$ enhances ${\beta}2AR$ signaling in osteoblasts. $TNF{\alpha}$ was further found in C2C12 cells to suppress bone morphogenetic protein 2-induced alkaline phosphatase (ALP) activity and the expression of osteogenic marker genes including Runx2, ALP and osteocalcin. Propranolol, a ${\beta}2AR$ antagonist, attenuated this $TNF{\alpha}$ suppression of osteogenic differentiation. $TNF{\alpha}$ increased the expression of receptor activator of NF-${\kappa}B$ ligand (RANKL), an essential osteoclastogenic factor, in C2C12 cells which was again blocked by propranolol. In summary, our data show that $TNF{\alpha}$ increases ${\beta}2AR$ expression in osteoblasts and that a blockade of ${\beta}2AR$ attenuates the suppression of osteogenic differentiation and stimulation of RANKL expression by $TNF{\alpha}$. These findings imply that a crosstalk between $TNF{\alpha}$ and ${\beta}2AR$ signaling pathways might occur in osteoblasts to modulate their function.