The effects of static and intermittent compression on nitric oxide production in articular cartilage explants

Fermor, Beverley; Weinberg, J. Brice; Pisetsky, David S.; Misukonis, Mary A.; Banes, Albert J.; Guilak, Farshid

doi:10.1016/s0736-0266(00)00049-8

Cited by 148 publications

(114 citation statements)

References 36 publications

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“…It is important to note that these experiments were primarily designed to measure matrix metabolism and the production of inflammatory mediators in response to a steadystate mechanical stimulus. Our previous studies have shown that this mechanical regimen significantly increases NO and PGE 2 production by porcine meniscus or articular cartilage without loss of cell viability (17,19).…”

Section: Discussionmentioning

confidence: 88%

“…Compressive loads were applied to 24 samples simultaneously by using a modified version of the Biopress system as described previously (17)(18)(19). Compression experiments were performed for 24 h at a frequency of 0.5 Hz (square wave with 1 s on and 1 s off) at a magnitude of 0.1 MPa.…”

Section: Methodsmentioning

confidence: 99%

“…IL-1 also induces production of NO from lapine and human osteoarthritic menisci (5,34). Mechanical stress increases NO production through a NOS2-dependent mechanism in cartilage (9,17,18,20,32,33) and meniscus (19). It is of particular interest that cyclic tensile stretch can exert a protective effect on IL-1-induced matrix degradation in fibrochondrocytes from the temporomandibular joint (1).…”

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confidence: 99%

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Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide

Shin¹,

Fermor²,

Weinberg³

et al. 2003

Journal of Applied Physiology

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. Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide. J Appl Physiol 95: 308-313, 2003. First published March 28, 2003 10.1152/ japplphysiol.00131.2003The meniscus is an intra-articular fibrocartilaginous structure that serves essential biomechanical roles in the knee. With injury or arthritis, the meniscus may be exposed to significant changes in its biochemical and biomechanical environments that likely contribute to the progression of joint disease. The goal of this study was to examine the influence of mechanical stress on matrix turnover in the meniscus in the presence of interleukin-1 (IL-1) and to determine the role of nitric oxide (NO) in these processes. Explants of porcine menisci were subjected to dynamic compressive stresses at 0.1 MPa for 24 h at 0.5 Hz with 1 ng/ml IL-1, and the synthesis of total protein, proteoglycan, and NO was measured. The effects of a nitric oxide synthase 2 (NOS2) inhibitor were determined. Dynamic compression significantly increased protein and proteoglycan synthesis by 68 and 58%, respectively, compared with uncompressed explants. This stimulatory effect of mechanical stress was prevented by the presence of IL-1 but was restored by specifically inhibiting NOS2. Release of proteoglycans into the medium was increased by IL-1 or mechanical compression and further enhanced by IL-1 and compression together. Stimulation of proteoglycan release in response to compression was dependent on NOS2 regardless of the presence of IL-1. These finding suggest that IL-1 may modulate the effects of mechanical stress on extracellular matrix turnover through a pathway that is dependent on NO.

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Section: Discussionmentioning

confidence: 88%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide

Shin¹,

Fermor²,

Weinberg³

et al. 2003

Journal of Applied Physiology

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“…Under physical stress, changes in gene expression and an increase in production of inflammatory cytokines and matrix-degrading enzymes have been noted in the cartilaginous tissue. 166 All these biochemical findings have generated a controversy about the inflammatory nature of the condition (similar to the case with keratoconous). It has been proposed that although the disorder does not meet the definition of inflammatory, based on the numbers of leukocytes in synovial fluid, the presence of proinflammatory mediators, which perpetuate disease progression, warrants a reconsideration of the definition of inflammation.…”

Section: Resultsmentioning

confidence: 99%

Keratoconus: an inflammatory disorder?

Galvis

Sherwin

Tello

et al. 2015

Eye

302

199

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Keratoconus has been classically defined as a progressive, non-inflammatory condition, which produces a thinning and steepening of the cornea. Its pathophysiological mechanisms have been investigated for a long time. Both genetic and environmental factors have been associated with the disease. Recent studies have shown a significant role of proteolytic enzymes, cytokines, and free radicals; therefore, although keratoconus does not meet all the classic criteria for an inflammatory disease, the lack of inflammation has been questioned. The majority of studies in the tears of patients with keratoconus have found increased levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase (MMP)-9. Eye rubbing, a proven risk factor for keratoconus, has been also shown recently to increase the tear levels of MMP-13, IL-6, and TNF-α. In the tear fluid of patients with ocular rosacea, IL-1α and MMP-9 have been reported to be significantly elevated, and cases of inferior corneal thinning, resembling keratoconus, have been reported. We performed a literature review of published biochemical changes in keratoconus that would support that this could be, at least in part, an inflammatory condition.

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“…Several studies investigated the effect of mechanical stimulation on chondrocyte metabolism. In general, static compression decreases biosynthetic activity compared to unloaded tissue while dynamic compression has been found to stimulate, inhibit or have no effect on biosynthetic activity depending on the loading frequency and amplitude [13][14][15]. Other studies have shown that cyclic tensile strains of low magnitude (3-8% equibiaxial strain) and physiological levels of cyclic compressive forces (15% compression) elicit an anabolic response [16,17], while strains of high magnitude (10-15% equibiaxial strain) initiate cartilage damage.…”

Section: Introductionmentioning

confidence: 99%

Validation of an In Vitro Model to Study Human Cartilage Responses to Compression

Isla¹,

Huselstein²,

Mainard³

et al. 2012

ENG

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The aim of this work was to develop an in vitro model to study mechanical compression effects on cartilage. A pressure-controlled compression device was used in this study. Cartilage explants obtained from human knee were compressed at 1MPa/1Hz for 7 hours (30 min ON, 30 min OFF) under normoxia (5% CO 2 , 21% O 2 ) or hypoxia (5% CO 2 , 5% O 2 ). Cell viability was analyzed while nitric oxide (NO) and glycosaminoglycans (GAG) release was assayed in culture media. Mechanical stimulation increased NO production and GAG release by human cartilage explants under normoxia and hypoxia culture. In normoxia and hypoxia conditions, mechanical stimulation alters human OA cartilage metabolism. There is also, an increase in matrix degradation after compression, as shown by levels of GAG found in culture media. This study put in evidence the importance of mechanical compression in the progression of the osteoarthritis and present and in vitro model for mechanobiological and pharmacological studies.

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The effects of static and intermittent compression on nitric oxide production in articular cartilage explants

Cited by 148 publications

References 36 publications

Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide

Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide

Keratoconus: an inflammatory disorder?

Validation of an In Vitro Model to Study Human Cartilage Responses to Compression

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