| Co-Investigator(Kenkyū-buntansha) |
FUJII Akira Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (70102564)
AKIMOTO Yoshiaki Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (10147720)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
In order to clarify the mechanism of oral disease, it is quite important to know an interaction between epithelium and fibroblast and its characteristics on signal transduction in oral tissue. Ets factors constitute one important class of transcriptional regulators that play critical roles in hematopoiesis, angiogenesis, organogenesis, oncogenesis, and specification of neuronal connectivity. These proteins are expressed mainly in hematopoietic cells, however, some are also expressed in epithelial cells. The present study was investigated Ets gene family, Epithelium-specific ets transcription factor, family member-1,-2, and-3 (ESE-1,-2,and-3), expression and regulation in buccal mucosa carcinoma-derived cell line, HO-1-N-1,epithelial-like cell. HO-1-N-1 cell itself showed ESE-1,-2 and-3 mRNA expression in the absence of stimulant. IL-1α and IL-1β increased ESE-3 mRNA expression in a dose-dependent manner, however, they did not clearly alter ESE-1 and-2 mRNA expression. Phorbol 12-myristate 13-acetate (PMA) also increased ESE-3 mRNA expression in a dose-dependent manner, and ESE-3 mRNA expression enhanced by PMA was inhibited by PKC inhibitor (bisindolylmaleimide, BIS) and MEK1/2 inhibitor (U0126). These results suggest that ESE-3 might be an important determinant in an inflammation process. In addition, ESE-3 mRNA expression enhanced by PKC activator is regulated through MEK1/2 pathway in HO-1-N-1 cell.
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