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KMID : 0829220110350030161
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Korean Journal of Oral and Maxillofacial Pathology
2011 Volume.35 No. 3 p.161 ~ p.166
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Involvement of MAP Kinase on Nicotine- and LPS-induced Human Beta Defensin-2 Expression in Periodontal Ligament Cells
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Lee Sang-Im
Lee Hwa-Jeong
Bae Won-Jung
Kang Sun-Il
Lee So-Yun
Lee Young-Man
Shin Kyung-Sub
Park Jae-Kook
Ryu Won-Kook
Chae Jong-Moon
Kim Eun-Cheol
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Abstract
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Human β- defensin-2 (hBD-2) is an antimicrobial peptide which is produced by epithelial cells after stimulation with microorganisms or inflammatory mediators. However, little is known as to whether the LPS and nicotine induces the expression of hBD-2 in periodontal l igament (PDL) cells. T he p urpose o f this s tudy was t o investigate t he r oles o f MAPKs pathway o f nicotine a nd L PS-induced hBD-2 expression in PDL cells. The maximal expression of hBD-2 was observed in nicotine 5 mM and LPS 1 ㎍/㎖ treated PDL cells. Nicotine and LPS induced the phosphorylation of p38, c-Jun N-terminal kinase 1 and 2 (JNK1/2), and extracellular signal-regulated kinases 1 and 2 (ERK1/2) MAPK. ERK1/2 inhibitor SB203580, p38 inhibitor PD98059, and JNK inhibitor SP600125, blocked the effects of nicotine and LPS on hBD-2 upregulation in PDL cells. These results collectively suggest that hBD-2 is up-regulated in nicotine and LPS-treated PDL cells through activation of p38, ERK and JNK MAPKs pathway. Our data regarding the up-regulation of hBD-2 may help us to understand the antimicrobial mechanism in periodontal disease.
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KEYWORD
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hBD-2, LPS, Nicotine, PDL cells
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