Intermittent hydrostatic pressure inhibits matrix metalloproteinase and pro-inflammatory mediator release from human osteoarthritic chondrocytes in vitro

Trindade, Michael C. D.; Shida, Junichi; Ikenoue, Takashi; Lee, Mel S.; Lin, Eric Y; Yaszay, Burt; Yerby, Scott A.; Goodman, Stuart B.; Schurman, David J.; Smith, Robert L.

doi:10.1016/j.joca.2004.05.008

Cited by 43 publications

(29 citation statements)

References 41 publications

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“…High strain, which produced matrix disruption that included severe fiber angulation and longitudinal fiber separation and increased MMP-13 level, were consistent with those of late-stage clinical tendinopathy [16,20,21,27,37]. By contrast, low strain, which or similar pathologic conditions [1,40,48]. We have observed similar suppressive effects on MMP expression in chondrocytes [49], and comparable mechanisms may apply in tendon.…”

Section: Discussionsupporting

confidence: 77%

Coordinate Regulation of IL-1β and MMP-13 in Rat Tendons Following Subrupture Fatigue Damage

Sun

Fung

et al. 2008

Clinical Orthopaedics &Amp; Related Research

101

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Mechanical overloading is a major causative factor of tendinopathy; however, its underlying mechanisms are unclear. We hypothesized mechanical overloading would damage tendons and alter genes associated with tendinopathy in a load-dependent manner. To test this hypothesis, we fatigue loaded rat patellar tendons in vivo and measured expression of the matrix-degrading enzyme MMP-13 and the inflammatory cytokine IL-1b. We also examined these responses in cultured tenocytes exposed to intermittent hydrostatic pressure in vitro. Additionally, we hypothesized load-induced changes in tenocyte MMP-13 expression would be dependent on expression of IL-1b. In vivo fatigue loading at 1.7% strain caused overt microstructural damage and upregulated expression of MMP-13 and IL-1b, while 0.6% strain produced only minor changes in matrix microstructure and downregulated expression of both MMP-13 and IL-1b. Loading of cultured tenocytes at 2.5 and 7.5 MPa produced comparable changes in expression to those of in vivo tendon loading. Blocking IL-1b expression with siRNA suppressed load-induced both MMP-13 mRNA expression and activity. The data suggest fatigue loading alters expression of MMP-13 and IL-1b in tendons in vivo and tenocytes in vitro in a load-dependent manner. The data also suggest MMP-13 is regulated by both IL-1b-dependent and IL-1b-independent pathways.

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Section: Discussionsupporting

confidence: 77%

Coordinate Regulation of IL-1β and MMP-13 in Rat Tendons Following Subrupture Fatigue Damage

Sun

Fung

et al. 2008

Clinical Orthopaedics &Amp; Related Research

101

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“…Therefore, the effects of the cytokine alone could not account for these complex conditions of OA in vivo. Up-regulation of MMP-2 mRNA might be the result of other factors, including hypoxia/reoxygenation, cell-matrix interactions, and intermittent hydrostatic pressures (44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

Comparative analysis of gene expression profiles in intact and damaged regions of human osteoarthritic cartilage

Sato

Konomi

Yamasaki

et al. 2006

Arthritis & Rheumatism

154

130

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Objective. To analyze the differences in gene expression profiles of chondrocytes in intact and damaged regions of cartilage from the same knee joint of patients with osteoarthritis (OA) of the knee.Methods. We compared messenger RNA expression profiles in regions of intact and damaged cartilage (classified according to the Mankin scale) obtained from patients with knee OA. Five pairs of intact and damaged regions of OA cartilage were evaluated by oligonucleotide array analysis using a double in vitro transcription amplification technique. The microarray data were confirmed by real-time quantitative polymerase chain reaction (PCR) amplification and were compared with previously published data.Results. About 1,500 transcripts, which corresponded to 8% of the expressed transcripts, showed >2-fold differences in expression between the cartilage tissue pairs. Approximately 10% of these transcripts (n ‫؍‬ 151) were commonly expressed in the 5 patient samples. Accordingly, 114 genes (35 genes expressed in intact > damaged; 79 genes expressed in intact < damaged) were selected. The expression of some genes related to the wound-healing process, including cell proliferation and interstitial collagen synthesis, was higher in damaged regions than in intact regions, similar to the findings for genes that inhibit matrix degradation. Comparisons of the real-time quantitative PCR data with the previously reported data support the validity of our microarray data.Conclusion. Differences between intact and damaged regions of OA cartilage exhibited a similar pattern among the 5 patients examined, indicating the presence of common mechanisms that contribute to cartilage destruction. Elucidation of this mechanism is important for the development of effective treatments for OA.

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“…(27,28)] on the pressures and pressure-time cycles cartilage experience in life are essential to understanding the etiology of osteoarthritis, as in research on the influence of pressure at matrix, cellular, and subcellular scales (8,56,57). These in vivo pressures also define the pressure environment that proposed augmentations to, and substitutions for, natural cartilage must endure for the subsequent life of the joint.…”

Section: Discussionmentioning

confidence: 99%

Corroboration of in vivo cartilage pressures with implications for synovial joint tribology and osteoarthritis causation

Morrell

Hodge

Krebs

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

102

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Pressures on normal human acetabular cartilage have been collected from two implanted instrumented femoral head hemiprostheses. Despite significant differences in subjects' gender, morphology, mobility, and coordination, in vivo pressure measurements from both subjects covered similar ranges, with maximums of 5-6 MPa in gait, and as high as 18 MPa in other movements. Normalized for subject weight and height (nMPa), for free-speed walking the maximum pressure values were 25.2 for the female subject and 24.5 for the male subject. The overall maximum nMPa values were 76.2 for the female subject during rising from a chair at 11 months postoperative and 82.3 for the male subject while descending steps at 9 months postoperative. These unique in vivo data are consistent with corresponding cadaver experiments and model analyses. The collective results, in vitro data, model studies, and now corroborating in vivo data support the self-pressurizing ''weeping'' theory of synovial joint lubrication and provide unique information to evaluate the influence of in vivo pressure regimes on osteoarthritis causation and the efficacy of augmentations to, and substitutions for, natural cartilage.

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Intermittent hydrostatic pressure inhibits matrix metalloproteinase and pro-inflammatory mediator release from human osteoarthritic chondrocytes in vitro

Abstract: IHP decreased release of MMP-2, IL-6 and MCP-1 by osteoarthritic chondrocytes in vitro suggesting that pressure influences cartilage stability by modulating chondrocyte expression of these degradative and pro-inflammatory proteins in vivo.

Cited by 43 publications

References 41 publications

Coordinate Regulation of IL-1β and MMP-13 in Rat Tendons Following Subrupture Fatigue Damage

Coordinate Regulation of IL-1β and MMP-13 in Rat Tendons Following Subrupture Fatigue Damage

Comparative analysis of gene expression profiles in intact and damaged regions of human osteoarthritic cartilage

Corroboration of in vivo cartilage pressures with implications for synovial joint tribology and osteoarthritis causation

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