Enhanced expression of interleukin-6, matrix metalloproteinase-13, and receptor activator of NF-κB ligand in cells derived from osteoarthritic subchondral bone

Sakao, Kei; Takahashi, Kenji; Mazda, Osam; Tonomura, Hitoshi; Saito, Motoki; Fujioka, Mikihiro; Takamiya, Hisatake; Imanishi, Jirô; Kubo, Toshikazu

doi:10.1007/s00776-008-1227-5

Cited by 34 publications

(24 citation statements)

References 28 publications

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“…A possible mechanism is the elevated MMP-9 secretion induced by higher IL-6 expression from monocytes, which is activated by the synovial inflammatory response, thereby disturbing the balance between MMPs and TIMPs and leading to the damage of chondrocytes (Guo et al, 2011). In this process, IL-6 stimulates the production of prostaglandin and collagenase in normal cartilage and synovial cells in order to stimulate the IL-1 induced-MMP response in synovial fibroblasts in rheumatoid arthritis (Litinsky et al, 2006;Wang et al, 2010;Shen et al, 2011) or to elevate the expression of VEGF (vascular endothelial growth factor) type II receptor, thus facilitating MMP-9 secretion (Sakao et al, 2008;Kim et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…Knee OA was diagnosed based on the following 1986 American Rheumatism Association guidelines (Sakao et al, 2008): 1) prolonged knee pain in the past month; 2) crepitus during knee movement; 3) morning stiffness lasting <30 min; 4) knee tissue swelling with snapping sounds from joint; 5) knee tissue swelling without snapping sounds; and 6) serological test. Knee OA diagnosis was made on the basis of occurrence of a combination of characteristics (1) + (2) + (3) + (4) or (1) + (2) + (3) + (5) or (1) + (6) and X-ray examinations using the Kellgren-Lawrence classification grades.…”

Section: Diagnostic Criteriamentioning

confidence: 99%

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Correlation between interleukin-6 expression in articular cartilage bone and osteoarthritis

Qu¹,

Wang²,

Tang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. This study aimed to investigate the expressional profile of interleukin-6 (IL-6) in articular cartilage bone of osteoarthritis (OA) patients and its correlation with OA. A total of 30 articular cartilage bone samples from knee OA patients, which were collected by knee arthroscopy or articular surgery, comprised the study group, and 30 samples of normal articular cartilage tissue comprised the control group. Both mRNA (messenger ribonucleic acid) and protein levels of IL-6 and matrix metalloproteinase-9 (MMP-9) were measured and compared, and a correlation analysis was performed between the two. The integral optical density (IOD) values of MMP-9 and IL-6 proteins in the study group were 9.21 ± 3.22 and 8.94 ± 3.17, respectively; these were significantly higher (P < 0.05) than those in the control group at 3.14 ± 1.48 and 6.64 ± 1.53, respectively. The IOD values of mRNA transcripts for MMP-9 and IL-6 in the study group were 8.31 ± 2.28 and 8.78 ± 3.43, respectively; these were significantly higher than the values in the control group at 3.52 ± 1.37 and 5.21 ± 1.72 (P < 0.05), respectively. Further, the correlation analysis revealed significantly positive relationships for both protein (r = 0.434, P = 0.001) and mRNA (r = 14190 X.Q. Qu et al.©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 14189-14195 (2015) 0.413, P = 0.002) levels between MMP-9 and IL-6. In conclusion, articular cartilage tissues in knee OA patients have higher levels of MMP-9 and IL-6 expression, and these may play a synergistic role in OA pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Diagnostic Criteriamentioning

confidence: 99%

Correlation between interleukin-6 expression in articular cartilage bone and osteoarthritis

Qu¹,

Wang²,

Tang³

et al. 2015

Genet. Mol. Res.

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“…NF-κB is a homogeneous or heterogeneous protein dimer consisting of p50 and p65 Rel family proteins (22). The affinity of NF-κB for DNA is regulated by a group of inhibitory proteins of the IκB family, including IκB-·, IκB-ß, IκB-Á, IκB-‰, IκB-Â and BCL-3.…”

Section: Discussionmentioning

confidence: 99%

In vitro study of inhibitory millimeter wave treatment effects on the TNF-α-induced NF-κB signal transduction pathway

Wu²,

Wu³

et al. 2010

Int J Mol Med

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Abstract. Abnormal activation of the nuclear factor-κB (NF-κB) in chondrocytes initiates the transcription of inflammatory mediators, promotes their generation and release, and amplifies initial inflammatory signals. This results in the release of chondral matrix-degrading enzymes and accelerates the degeneration of articular cartilage. As a non-pharmaceutical and non-invasive physical therapy regimen, millimeter wave treatment has been successfully used for the treatment of osteoarthritis. In this study, chondrocytes were derived from the cartilages of knee joints of 4-week-old male Sprague-Dawley rats and were mechanically digested by collagenase type II treatment for further culture in vitro. The third-passage chondrocytes were stained with toluidine blue and treated with a gradient of tumor necrosis factor-· (TNF-·) for various times. Chondrocytic activity was measured by MTT assay, and the apoptotic rate of the chondrocytes was determined with Hocehst 33342 staining to identify effective treatment concentrations and durations and to establish an apoptosis model for the chondrocytes in response to TNF-·. Using this model, the chondrocytes were randomly divided to receive millimeter wave treatment for various times. The apoptotic rate of the chondrocytes was measured by Annexin V-FITC staining and the protein expression levels of RIP, TAK1, IκB kinase (IKK)-ß, IκB-· and NF-κB, were determined by Western blotting. Chondrocytic structure was examined by transmission electronic microscopy. The apoptotic rates were significantly lower at 4 and 8 h of treatment than at 0 and 2 h. The expression levels of RIP, TAK1, IKK-ß and NF-κB were also significantly lower at 4 and 8 h than at 0 and 2 h, whereas that of IκB-· was significantly higher at 4 and 8 h than at 0 and 2 h. Therefore, we can conclude that millimeter wave treatment can inhibit the activation of the TNF-·-mediated NF-κB signal transduction pathway through the down-regulation of RIP, TAK1, IKK-ß and NF-κB, and the up-regulation of IκB-·, in chondrocytes.

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“…Reverse transcriptasepolymerase chain reaction (RT-PCR) was performed as described, using specific primer sets for P-ATPase (5′-CCCTACTATGGCAAGAAAGCAC-3′ [forward] and 5′-TCACGTGAGGGTTGGTGATACT-3′ [reverse]) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH; 5′-ACTGCCATCTGCTCTCCACTTG-3′ [forward] and 5′-CCTGGAAGATGGTGATGGGCTT-3′ [reverse]) [7]. The amplified products were separated by electrophoresis on 1.5% agarose gels and viewed under ultraviolet light.…”

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

Lansoprazole Inhibits Nitric Oxide and Prostaglandin E2 Production in Murine Macrophage RAW 264.7 Cells

et al. 2011

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Aberrantly activated macrophages, which overproduce inflammatory mediators, are involved in the pathogenesis of many inflammatory diseases. We analyzed the anti-inflammatory activity of lansoprazole (LPZ), a typical proton pump (P-ATPase) inhibitor, on RAW264.7 murine macrophages. Treatment of lipopolysaccharide (LPS)-stimulated RAW264.7 cells with LPZ inhibited the production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)). Since P-ATPase expression was not observed in RAW264.7 cells, the anti-inflammatory effect of LPZ was independent of ATPase. In contrast, diphenylene iodonium (DPI), an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, decreased NO but not PGE(2) levels. LPZ suppressed the LPS-stimulated production by RAW264.7 cells of reactive oxygen species (ROS), which plays an important role in inflammatory responses. ROS elevation in these cells was associated with NO but not PGE(2) production, suggesting that LPZ inhibits NO production by suppressing NADPH oxidase activity. These findings suggest that LPZ may be useful in the treatment of many inflammatory diseases associated with activated macrophages.

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Enhanced expression of interleukin-6, matrix metalloproteinase-13, and receptor activator of NF-κB ligand in cells derived from osteoarthritic subchondral bone

Cited by 34 publications

References 28 publications

Correlation between interleukin-6 expression in articular cartilage bone and osteoarthritis

Correlation between interleukin-6 expression in articular cartilage bone and osteoarthritis

In vitro study of inhibitory millimeter wave treatment effects on the TNF-α-induced NF-κB signal transduction pathway

Lansoprazole Inhibits Nitric Oxide and Prostaglandin E2 Production in Murine Macrophage RAW 264.7 Cells

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