Matrix remodeling response of human periodontal tissue cells toward fibrosis upon nicotine exposure

被引:14
作者
Takeuchi-Igarashi, Hiroko [1 ,2 ]
Kubota, Satoshi [3 ]
Tachibana, Toshiaki [4 ]
Murakashi, Etsuko [1 ]
Takigawa, Masaharu [3 ]
Okabe, Masataka [2 ]
Numabe, Yukihiro [1 ]
机构
[1] Nippon Dent Univ Tokyo, Sch Life Dent Tokyo, Dept Periodontol, Chiyoda Ku, 1-9-20 Fujimi, Tokyo 1028159, Japan
[2] Jikei Univ, Dept Anat, Sch Med, Tokyo 105, Japan
[3] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Biochem & Mol Dent, Okayama, Japan
[4] Jikei Univ, Core Res Facil, Sch Med, Div Fine Morphol, Tokyo, Japan
关键词
Fibrosis; Gingival fibrosis; Matrix remodeling; Nicotine; Smoking; HUMAN GINGIVAL FIBROBLASTS; FIBROTIC HUMAN LIVER; CIGARETTE-SMOKING; EXTRACELLULAR-MATRIX; EXPRESSION; METALLOPROTEINASES; INHIBITOR; SMOKERS; TOBACCO; PROLIFERATION;
D O I
10.1007/s10266-014-0177-y
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
It is widely accepted that fibrosis is frequently observed in the gingiva of smokers. However, the mechanisms by which smoking results in pathological changes in periodontal tissue that lead to fibrosis are not entirely clear. Our former report showed that type I collagen synthesis was promoted by nicotine via CCN family protein 2 in human periodontal tissue cells. Here, we evaluated other aspects of nicotine function from a viewpoint of extracellular matrix (ECM) remodeling. Human gingival fibroblasts (n = 4) and periodontal ligament cells (n = 3) were isolated. The cells were treated with nicotine at a variety of concentrations for 12-48 h. Modulators of matrix remodeling were measured using enzyme-linked immunosorbent assays. Cell migration and morphology were also evaluated. As a result, following treatment with 1 mu g/ml nicotine, tissue inhibitor of metalloproteinase-1 and transforming growth factor-beta 1 production in both cell lysates and supernatants, and matrix metalloproteinases-1 production in cell lysates, were significantly increased (p < 0.05). Compared to controls, cell migration was significantly inhibited (p < 0.005) by nicotine in a time-dependent manner. Electron microscopic analysis revealed the presence of a number of vacuoles in nicotine-treated cells. These results indicate that nicotine not only impairs fibroblast motility, and induces cellular degenerative changes, but also alters ECM-remodeling systems of periodontal cells. Induction of matrix remodeling molecules, combined with type I collagen accumulation, may account for the molecular mechanism of nicotine-induced periodontal fibrosis.
引用
收藏
页码:35 / 43
页数:9
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