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KMID : 0848120130380010037
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International Journal of Oral Biology
2013 Volume.38 No. 1 p.37 ~ p.42
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NFATc1 and NFATc3 is Involved in the Expression of Receptor Activator of NF-κB Ligand in Activated T Lymphocytes
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Baek Jeong-Hwa
Heo Sun-Jae
Park Hyun-Jung
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Abstract
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Receptor activator of NF-κB ligand (RANKL) is an essential cytokine for osteoclast differentiation, activation and survival. T lymphocytes such as T17 cells, a subset of T helper cells that produce IL-17, play an important role in rheumatoid arthritic bone resorption by producing inflammatory cytokines and RANKL. It has not yet been clearly elucidated how T cell activation induces RANKL expression. T cell receptor activation induces the activation of nuclear factor of activated T cell (NFAT) and expression of its target genes. In this study, we examined the role of NFAT in T cell activation- induced RANKL expression. EL-4, a murine T lymphocytic cell line, was used. When T cell activation was induced by phorbol 12-myristate 13-acetate (PMA) and ionomycin, RANKL expression increased in a time-dependent manner. In the presence of cyclosporin, an inhibitor of NFAT activation, this PMA/ionomycin?induced RANKL expression was blocked. Overexpression of either NFATc1 or NFATc3 induced RANKL expression. Chromatin immunoprecipitation results demonstrated that PMA/ionomycin treatment induced the binding of NFATc1 and NFATc3 to the mouse RANKL gene promoter. These results suggest that NFATc1 and NFATc3 mediates T cell receptor activationinduced RANKL expression in T lymphocytes.
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KEYWORD
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RANK ligand, T lymphocyte, NFATc1, NFATc3
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