Interleukin-1 stimulates cytokines, prostaglandin E and matrix metalloproteinase-1 production via activation of MAPK/AP-1 and NF-?B in human gingival fibroblasts

Prostaglandin E2 (PGE2) exerts its biological actions via EP receptors (EP1, EP2, EP3, and EP4). In the present study, we investigated whether PGE2 regulated interleukin (IL)-1β-induced matrix metalloproteinase (MMP)-3 production in human gingival fibroblasts (HGF) derived from periodontally healthy subjects and diseased patients. In HGF from healthy gingiva, PGE2 down-regulated IL-1β-induced MMP-3 production, whereas in HGF from periodontitis patients, PGE2 enhanced it. Butaprost (an EP2 agonist) and ONO-AE1-329 (an EP4 agonist) suppressed IL-1β-induced MMP-3 production, and 17-phenyl-ω-trinor PGE2 (an EP1 agonist) mimicked the PGE2 effect in HGF from healthy and periodontally diseased tissues, respectively. Analysis of these data suggests that, in HGF from healthy tissue, IL-1β-induced MMP-3 production is down-regulated by PGE2 via EP2 and EP4 receptors, whereas in cells from periodontally diseased tissue, IL-1β-induced MMP-3 production is up-regulated via EP1 receptors. Different regulation of IL-1β-induced MMP-3 production by PGE2 between healthy and periodontally diseased tissues may be involved in the pathogenesis of periodontal disease.

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Matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 production in human gingival fibroblasts: the role of protein kinase C

Journal of Periodontal Research ◽

10.1111/j.1600-0765.2004.00745.x ◽

2004 ◽

Vol 39 (5) ◽

pp. 308-314 ◽

Cited By ~ 19

Author(s):

H. Domeij ◽

T. Modeer ◽

T. Yucel-Lindberg

Keyword(s):

Protein Kinase C ◽

Protein Kinase ◽

Matrix Metalloproteinase ◽

Human Gingival Fibroblasts ◽

Tissue Inhibitor Of Metalloproteinase ◽

Gingival Fibroblasts ◽

Tissue Inhibitor ◽

Kinase C ◽

Matrix Metalloproteinase 1

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Therapeutic Effect of Chenodeoxycholic Acid in an Experimental Rabbit Model of Osteoarthritis

Mediators of Inflammation ◽

10.1155/2015/780149 ◽

2015 ◽

Vol 2015 ◽

pp. 1-7 ◽

Cited By ~ 2

Author(s):

Zhao-wei Yan ◽

Ji Dong ◽

Chen-hao Qin ◽

Chun-yang Zhao ◽

Li-yan Miao ◽

...

Keyword(s):

Matrix Metalloproteinase ◽

Therapeutic Effect ◽

Chenodeoxycholic Acid ◽

Cruciate Ligament ◽

Interleukin 1 ◽

Rabbit Model ◽

Bone Destruction ◽

Joint Disease ◽

Prostaglandin E ◽

Matrix Metalloproteinase 1

Osteoarthritis (OA) is a slowly progressive joint disease typically seen in middle-age to elderly people. At present, there is no ideal agent to treat OA. Chenodeoxycholic acid (CDCA) was a principal active constituent from animal bile. However, the therapeutic effect of CDCA on OA severity was largely unknown. The purpose of this study was to evaluate the therapeutic effect of intra-articular injection of CDCA in a rabbit OA model. OA was induced in experimental rabbits by anterior cruciate ligament transection (ACLT) and then rabbits were intra-articularly injected with CDCA (10 mg/kg or 50 mg/kg) once per week for 5 weeks. The results showed that CDCA significantly decreased cartilage degradation on the surface of femoral condyles, reducing the pathological changes of articular cartilage and synovial membrane by macroscopic and histological analysis. CDCA also significantly decreased bone destruction and erosion of joint evaluated by micro-CT. Furthermore, CDCA could markedly reduce the release of matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3), interleukin-1β(IL-1β), and prostaglandin E2(PGE2) in synovial fluid. These observations highlight CDCA might be a potential therapeutic agent for OA.

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