Celecoxib exerts protective effects on extracellular matrix metabolism of mandibular condylar chondrocytes under excessive mechanical stress

Su, Shao-Ching; Tanimoto, Kotaro; Tanne, Yuki; Kunimatsu, Ryo; Hirose, Naoto; Mitsuyoshi, Tomomi; Okamoto, Yuki; Tanne, Kazuo

doi:10.1016/j.joca.2014.03.011

Cited by 49 publications

(46 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Scale bars = 50 µm. (Su et al, 2014;Sumi et al, 2018;Yanoshita et al, 2018). In this study, high-magnitude cyclic tensile stress was applied on ATDC5 chondrocytes in a condition of 10% cell elongation for 24 h, which caused the upregulated expression of inflammatory cytokines and matrixdegrading enzymes (Figure 2).…”

Section: Discussionmentioning

confidence: 96%

“…We have been investigating the relationship between excessive mechanical stress and chondrogenic destruction. The cyclic tensile stress is associated with expression of many kinds of inflammatory cytokines and proteinase in chondrocytes (Su et al, ; Sumi et al, ; Yanoshita et al, ). In this study, high‐magnitude cyclic tensile stress was applied on ATDC5 chondrocytes in a condition of 10% cell elongation for 24 h, which caused the upregulated expression of inflammatory cytokines and matrix‐degrading enzymes (Figure ).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Protective effects of cilengitide on inflammation in chondrocytes under excessive mechanical stress

Hirose

Okamoto

Yanoshita

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

Chondrocytes constantly receive external stimuli, which regulates remodeling. An optimal level of mechanical stress is essential for maintaining chondrocyte homeostasis, however, excessive mechanical stress induces inflammatory cytokines and protease, such as matrix metalloproteinases (MMPs). Therefore, excessive mechanical stress is considered to be one of the main causes to cartilage destruction leading to osteoarthritis (OA). Integrins are well‐known as cell adhesion molecules and act as receptors for extracellular matrix (ECM), and are believed to control intracellular signaling pathways both physically and chemically as a mechanoreceptor. However, few studies have focused on the roles and functions of integrins in inflammation caused by excessive mechanical stress. In this study, we examined the relationship between integrins (αVβ3 and αVβ5) and the expression of inflammatory factors under mechanical loading in chondrocytes by using an integrin receptor antagonist (cilengitide). Cilengitide suppressed the gene expression of interleukin‐1β (IL‐1β), tumor necrosis factor‐α (TNF‐α), matrix metalloproteinase‐3 (MMP‐3), and MMP‐13 induced by excessive mechanical stress. In addition, the protein expression of IL1‐β and MMP‐13 was also inhibited by the addition of cilengitide. Next, we investigated the involvement of intracellular signaling pathways in stress‐induced integrin signaling in chondrocytes by using western blotting. The levels of p‐FAK, p‐ERK, p‐JNK, and p‐p38 were enhanced by excessive mechanical stress and the enhancement was suppressed by treatment with cilengitide. In conclusion, this study revealed that excessive mechanical stress may activate integrins αVβ3 and αVβ5 on the surface of chondrocytes and thereby induce an inflammatory reaction by upregulating the expression of IL‐1β, TNF‐α, MMP‐3, and MMP‐13 through phosphorylation of FAK and MAPKs.

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Protective effects of cilengitide on inflammation in chondrocytes under excessive mechanical stress

Hirose

Okamoto

Yanoshita

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

show abstract

“…To identify novel OA therapeutic approaches, we previously investigated the possibility of and mechanism underlying OA inflammation reduction by drug administration. Celecoxib, a selective COX-2 inhibitor, is known to exert protective effects on ECM metabolism in mandibular condylar chondrocytes under excessive mechanical stress [19]. Decactinib, a FAK inhibitor, and semaphorin 3A were shown to inhibit inflammation in chondrocytes under cyclic tensile strain (CTS) [20,21].…”

Section: Introductionmentioning

confidence: 99%

High-Frequency Near-Infrared Diode Laser Irradiation Attenuates IL-1β-Induced Expression of Inflammatory Cytokines and Matrix Metalloproteinases in Human Primary Chondrocytes

Sakata

Kunimatsu

Tsuka

et al. 2020

JCM

View full text Add to dashboard Cite

High-frequency near-infrared diode laser provides a high-peak output, low-heat accumulation, and efficient biostimulation. Although these characteristics are considered suitable for osteoarthritis (OA) treatment, the effect of high-frequency near-infrared diode laser irradiation in in vitro or in vivo OA models has not yet been reported. Therefore, we aimed to assess the biological effects of high-frequency near-infrared diode laser irradiation on IL-1β-induced chondrocyte inflammation in an in vitro OA model. Normal Human Articular Chondrocyte-Knee (NHAC-Kn) cells were stimulated with human recombinant IL-1β and irradiated with a high-frequency near-infrared diode laser (910 nm, 4 or 8 J/cm2). The mRNA and protein expression of relevant inflammation- and cartilage destruction-related proteins was analyzed. Interleukin (IL) -1β treatment significantly increased the mRNA levels of IL-1β, IL-6, tumor necrosis factor (TNF) -α, matrix metalloproteinases (MMP) -1, MMP-3, and MMP-13. High-frequency near-infrared diode laser irradiation significantly reduced the IL-1β-induced expression of IL-1β, IL-6, TNF-α, MMP-1, and MMP-3. Similarly, high-frequency near-infrared diode laser irradiation decreased the IL-1β-induced increase in protein expression and secreted levels of MMP-1 and MMP-3. These results highlight the therapeutic potential of high-frequency near-infrared diode laser irradiation in OA.

show abstract

“…It is generally accepted that appropriate joint biomechanical loading is essential for cartilage anabolic metabolism 3 , while abnormal joint loading results in cartilage metabolism imbalance favoring catabolic metabolism and OA changes 4–8 . Abnormal joint loading could downregulate expression of proteoglycans and Collagen II and upregulate expression of inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α), and cartilage extracellular matrix degrading enzymes, such as a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and matrix metalloproteinases (MMPs) 9 . Several recent reports indicate that nuclear factor-kappaB p65 (NF-κB p65) could directly bind to the promoters of targeting genes encoding for cartilage degrading factors 10 , such as ADAMTS-5 11 , so NF-κB p65 is considered to play a vital role as a pro-catabolic and pro-apoptotic factor of chondrocyte during OA development 12 .…”

Section: Introductionmentioning

confidence: 99%

Systemic administration of strontium or NBD peptide ameliorates early stage cartilage degradation of mouse mandibular condyles

Liu

Yang

Liao

et al. 2016

Osteoarthritis and Cartilage

View full text Add to dashboard Cite

SUMMARY Objective To determine whether mandibular condylar cartilage degradation induced by experimentally abnormal occlusion could be ameliorated via systemic administration of strontium or NBD peptide. Methods Six-week-old female C57BL/6J mice were used. From the seventh day after mock operation or unilateral anterior crossbite (UAC) treatment, the control and UAC mice were further respectively pharmacologically treated for 2 weeks or 4 weeks of saline (CON + Saline and UAC + Saline groups), SrCl2 (CON + SrCl2 and UAC + SrCl2 groups) or NBD peptide (CON + NBD peptide and UAC + NBD peptide groups). Changes in condylar cartilage and subchondral bone were assessed 21 and 35 days after mock operation or UAC procedure by histology and micro-CT. Real-time PCR and/or immunohistochemistry (IHC) were performed to evaluate changes in expression levels of col2a1, aggrecan, ADAMTS-5, tnf-α, il-1β, nfkbia, nuclear factor-kappaB phospho-p65 in condylar cartilage, and rankl/rank/opg in both condylar cartilage and subchondral bone. Results Cartilage degradation with decreased col2a1 and aggrecan expression, and increased ADAMTS-5, tnf-α/il1-β, nfkbia and NF-κB phospho-p65 was observed in UAC + Saline groups. Subchondral bone loss with increased osteoclast numbers and decreased opg/rankl ratio was found in UAC + Saline groups compared to age-match CON + Saline groups. Cartilage degradation and subchondral bone loss were reversed by treatment of SrCl2 or NBD peptide while the same dosage in control mice induced few changes in condylar cartilage and subchondral bone. Conclusions The results demonstrate reverse effect of systemic administration of strontium or NBD peptide on UAC-induced condylar cartilage degradation and subchondral bone loss.

show abstract

Celecoxib exerts protective effects on extracellular matrix metabolism of mandibular condylar chondrocytes under excessive mechanical stress

Abstract: Celecoxib exerts protective effects on mandibular condylar chondrocytes under CTS stimulation by diminishing degradation and restoring synthesis of ECM.

Cited by 49 publications

References 36 publications

Protective effects of cilengitide on inflammation in chondrocytes under excessive mechanical stress

Protective effects of cilengitide on inflammation in chondrocytes under excessive mechanical stress

High-Frequency Near-Infrared Diode Laser Irradiation Attenuates IL-1β-Induced Expression of Inflammatory Cytokines and Matrix Metalloproteinases in Human Primary Chondrocytes

Systemic administration of strontium or NBD peptide ameliorates early stage cartilage degradation of mouse mandibular condyles

Contact Info

Product

Resources

About