PPARgamma Inhibits Inflammation through the Suppression of ERK1/2 Kinase Activity in Human Gingival Fibroblasts.
- Author:
Young Hee LEE
1
;
Dong Hoon KWAK
;
Min Soo KANG
;
Govinda BHATTARAI
;
Nan Hee LEE
;
Eun Chung JHEE
;
Ho Keun YI
Author Information
1. Department of Oral Biochemistry, School of Dentistry and Institute of Oral Bioscience, BK21 Program, Chonbuk National University, Korea. yihokn@chonbuk.ac.kr
- Publication Type:Original Article
- Keywords:
human gingival fibroblasts;
PPARgamma;
periodontal inflammation;
ERK1/2;
iNOS
- MeSH:
Fibroblasts;
Gingiva;
Humans;
Inflammation;
Intercellular Adhesion Molecule-1;
Matrix Metalloproteinase 2;
Metabolic Networks and Pathways;
NF-kappa B;
Nitric Oxide Synthase Type II;
Periodontal Diseases;
Phosphotransferases;
PPAR gamma;
Thiazolidinediones;
Vascular Cell Adhesion Molecule-1
- From:International Journal of Oral Biology
2010;35(1):27-33
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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. PPARgamma 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 PPARgamma 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/PPARgamma and rosiglitazone in same culture system showed reduced ICAM-1, VCAM-1, MMP-2, -9 and COX-2. Finally, the anti-inflammatory effects of PPARgamma 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 PPARgamma indeed has a pivotal role in gingival inflammation and may be a putative molecular target for future therapeutic strategies to control chronic periodontal disease.
