TY - JOUR
T1 - Nicotine-induced CCN2
T2 - From smoking to periodontal fibrosis
AU - Takeuchi, H.
AU - Kubota, S.
AU - Murakashi, E.
AU - Zhou, Y.
AU - Endo, K.
AU - Ng, P. S.
AU - Takigawa, M.
AU - Numabe, Y.
N1 - Funding Information:
This study was supported by grants-in-aid for Scientific Research from the Ministry of Education, Science, and Culture, Japan (20592437, 19109008, and 19592142).
PY - 2010/1
Y1 - 2010/1
N2 - Since fibrosis is observed in smokers gingiva, it was hypothesized that fibrosis was caused by nicotine in the periodontium. Therefore, in this study, we investigated the effects of nicotine on the induction of a profibrotic molecule, connective tissue growth factor (CCN2/CTGF), in human gingival fibroblasts (HGFs) and periodontal ligament (PDL) cells. With 1 μg/mL nicotine, vacuolization and attenuated proliferation were observed. Interestingly, 1 μg/mL nicotine increased the production of CCN2/CTGF protein in both cells without increasing mRNA expression. Furthermore, type I collagen mRNA and protein were also increased and were significantly blocked by a CCN2/CTGF neutralizing antibody. This is the first report to describe a relationship between nicotine and CCN2/CTGF in periodontal tissue cells. Analysis of our data also indicated that nicotine was cytotoxic, while it increased CCN2/CTGF and, eventually, type I collagen production. These findings suggest that periodontal fibrosis can be promoted by nicotine from smoking via effects on CCN2/CTGF.
AB - Since fibrosis is observed in smokers gingiva, it was hypothesized that fibrosis was caused by nicotine in the periodontium. Therefore, in this study, we investigated the effects of nicotine on the induction of a profibrotic molecule, connective tissue growth factor (CCN2/CTGF), in human gingival fibroblasts (HGFs) and periodontal ligament (PDL) cells. With 1 μg/mL nicotine, vacuolization and attenuated proliferation were observed. Interestingly, 1 μg/mL nicotine increased the production of CCN2/CTGF protein in both cells without increasing mRNA expression. Furthermore, type I collagen mRNA and protein were also increased and were significantly blocked by a CCN2/CTGF neutralizing antibody. This is the first report to describe a relationship between nicotine and CCN2/CTGF in periodontal tissue cells. Analysis of our data also indicated that nicotine was cytotoxic, while it increased CCN2/CTGF and, eventually, type I collagen production. These findings suggest that periodontal fibrosis can be promoted by nicotine from smoking via effects on CCN2/CTGF.
KW - CTGF
KW - Fibrosis
KW - Gingival.
KW - Nicotine
KW - Smoking
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U2 - 10.1177/0022034509353403
DO - 10.1177/0022034509353403
M3 - Article
C2 - 19966042
AN - SCOPUS:72449142340
SN - 0022-0345
VL - 89
SP - 34
EP - 39
JO - Journal of Dental Research
JF - Journal of Dental Research
IS - 1
ER -