Degenerative changes of articular cartilage in association with mechanical stimuli

Tanne, Kazuo

doi:10.1016/j.jdsr.2007.10.004

Cited by 9 publications

(5 citation statements)

References 81 publications

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“…It has been reported that excessive mechanical loading causes articular dysfunctions such as temporomandibular joint disorders (TMD) and osteoarthritis through the production of inflammatory cytokines [3,22,23]. Inflammation cytokines and mediators, such as IL-1b and PGE 2 , are well known to be involved in mechanical stretch-induced inflammation in articular tissues [24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

et al. 2011

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“…We previously investigated the mechanism involved in OA and reported that the protein lubricant superficial zone protein (SZP) localizes on the temporomandibular joint surface [12]. We also demonstrated that excessive mechanical loading lowers SZP production [13]; increases the friction coefficient; increases MMP-1, 3, and 9 production; and destroys substrates such as type II collagens, aggrecan, and hyaluronic acid [14,15].…”

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

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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.

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“…Several studies have shown that chondrocytes constantly receive external stimuli, which regulate remodeling (Ortega et al, ; Lee et al, ). An optimal level of mechanical stress is essential for maintaining chondrocyte homeostasis, however, excessive mechanical stress is considered to be one of the main causes of cartilage destruction leading to osteoarthritis (OA) (Tanne, ). Excessive loading onto cell surface induces inflammatory cytokines and protease, such as MMPs, in chondrocytes (Su et al, ; Asakawa‐Tanne et al, ).…”

Section: Introductionmentioning

confidence: 99%

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

Hirose

Okamoto

Yanoshita

et al. 2020

Cell Biology International

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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.

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Degenerative changes of articular cartilage in association with mechanical stimuli

Cited by 9 publications

References 81 publications

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

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

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

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