KMID : 0848120110360040173
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International Journal of Oral Biology 2011 Volume.36 No. 4 p.173 ~ p.178
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TNF¥á Increases the Expression of ¥â2 Adrenergic Receptors in Osteoblasts
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Baek Jeong-Hwa
Baek Kyung-Hwa Lee Hye-Lim Hwang Hyo-Rin Park Hyun-Jung Kwon A-Rang Abdul S. Qadir
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Abstract
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Tumor necrosis factor alpha (TNF¥á) is a multifunctional cytokine that is elevated in inflammatory diseases such as atherosclerosis, diabetes and rheumatoid arthritis. Recent evidence has suggested that ¥â2 adrenergic receptor(¥â2AR) activation in osteoblasts suppresses osteogenic activity. In the present study, we explored whether TNF¥á modulates ¥âAR expression in osteoblastic cells and whether this regulation is associated with the inhibition of osteoblast differentiation by TNF¥á. In the experiments, we used C2C12 cells, MC3T3- E1 cells and primary cultured mouse bone marrow stromal cells. Among the three subtypes of ¥âAR, ¥â2 and ¥â3AR were found in our analysis to be upregulated by TNF¥á. Moreover, isoproterenol-induced cAMP production was observed to be significantly enhanced in TNF¥á-primed C2C12 cells, indicating that TNF¥á enhances ¥â2AR signaling in osteoblasts.TNF¥á 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¥â2AR antagonist, attenuated this TNF¥á suppression of osteogenic differentiation. TNF¥á increased the expression ofreceptor activator of NF-¥êB ligand (RANKL), an essential osteoclastogenic factor, in C2C12 cells which was againblocked by propranolol. In summary, our data show that TNF¥á increases ¥â2AR expression in osteoblasts and that ablockade of ¥â2AR attenuates the suppression of osteogenic differentiation and stimulation of RANKL expression byTNF¥á. These findings imply that a crosstalk between TNF¥á
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KEYWORD
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TNF¥á, ¥â2 adrenergic receptor, osteoblasts
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