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International journal of oral biology : official journal of the Korean Academy of Oral Biology and the UCLA Dental Research Institute v.35 no.1, 2010년, pp.27 - 33   피인용횟수: 1
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$PPAR{\gamma}$ Inhibits Inflammation through the Suppression of ERK1/2 Kinase Activity in Human Gingival Fibroblasts

Lee, Young-Hee    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University   ); Kwak, Dong-Hoon    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University   ); Kang, Min-Soo    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University   ); Bhattarai, Govinda    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University   ); Lee, Nan-Hee    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University   ); Jhee, Eun-Chung    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University   ); Yi, Ho-Keun    (Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University  );
  • 초록

    Periodontal disease is a major oral disorder and comprises a group of infections that lead to inflammation of the gingiva and the destruction of periodontal tissues. $PPAR{\gamma}$ plays an important role in the regulation of several metabolic pathways and has recently been implicated in inflammatory response pathways. However, its effects on periodontal inflammation have yet to be clarified. In our current study, we evaluated the anti-inflammatory effects of $PPAR{\gamma}$ on periodontal disease. Human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) showed high levels of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-2 (MMP-2), and -9 (MMP-9). Moreover, these cells also showed upregulated activities for extracellular signal regulated kinase (ERK1/2), inducible nitric oxide synthase (iNOS) and cyclooxygnase-2. However, cells treated with Ad/ $PPAR{\gamma}$ and rosiglitazone in same culture system showed reduced ICAM-1, VCAM-1, MMP-2, -9 and COX-2. Finally, the anti-inflammatory effects of $PPAR{\gamma}$ appear to be mediated via the suppression of the ERK1/2 pathway and consequent inhibition of NF-kB translocation. Our present findings thus suggest that $PPAR{\gamma}$ indeed has a pivotal role in gingival inflammation and may be a putative molecular target for future therapeutic strategies to control chronic periodontal disease.


  • 주제어

    human gingival fibroblasts .   $PPAR{\gamma}$ .   periodontal inflammation .   ERK1/2 .   iNOS.  

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  • 이 논문을 인용한 문헌 (1)

    1. 2012. "" International journal of oral biology : official journal of the Korean Academy of Oral Biology and the UCLA Dental Research Institute, 37(3): 85~90     

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  • 이난희 (1)

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