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Effect of globular adiponectin on interleukin-6 and interleukin-8 expression in periodontal ligament and gingival fibroblasts

  • Park, Hong-Gyu (Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry) ;
  • Bak, Eun-Jung (Oral Cancer Research Institute, Yonsei University College of Dentistry) ;
  • Kim, Ji-Hye (Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry) ;
  • Lee, Yang-Sin (Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry) ;
  • Choi, Seong-Ho (Research Center for Orofacial Hard Tissue Regeneration, Yonsei University College of Dentistry) ;
  • Cha, Jeong-Heon (Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry) ;
  • Yoo, Yun-Jung (Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry)
  • Received : 2011.05.04
  • Accepted : 2011.05.21
  • Published : 2011.06.30

Abstract

Purpose: Globular adiponectin (gAd) is a type of adipocytokine, which is mainly produced by adipose tissue. It has been reported that gAd acts as a pro- as well as an anti-inflammatory factor. Interleukin (IL)-6 and IL-8 are pro-inflammatory cytokines. To investigate the role of gAd on periodontal tissues, the expression of adiponectin receptor 1 (AdipoR1) and the effect of gAd on the expression of IL-6 and IL-8 were investigated in periodontal ligament (PDL) and gingival fibroblasts. Methods: PDL and gingival fibroblasts were cultured from human periodontal tissues. gAd derived from Escherichia coli and murine myeloma cells were used. The expression of AdipoR1 was estimated by reverse transcription-polymerase chain reaction and western blot The expression of cytokines was measured by enzyme-linked immunosorbent assay. Results: PDL and gingival fibroblasts expressed both mRNA and protein of AdipoR1. gAd derived from E. coli increased the production of IL-6 and IL-8, but polymyxin B, an inhibitor of lipopolysaccharide (LPS), inhibited IL-6 and IL-8 production induced by gAd in both types of cells. gAd derived from murine myeloma cells did not induce IL-6 and IL-8 production in those cells. gAd derived from E. coli contained higher levels of LPS than gAd derived from murine myeloma cells. LPS increased production of IL-6 and IL-8 in PDL and gingival fibroblasts, but pretreatment of cells with gAd derived from murine myeloma cells did not inhibit LPS-induced IL-6 and IL-8 expression. Conclusions: Our results suggest that PDL and gingival fibroblasts express AdipoR1 and that gAd does not act as a modulator of IL-6 and IL-8 expression in PDL and gingival fibroblasts.

Keywords

References

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