Serum levels of collagenase, stromelysin‐1, and timp‐1

Manicourt, Daniel; Fujimoto, Noboru; Obata, Kenichi; Thonar, Eugene J.‐M.A.

doi:10.1002/art.1780371211

Cited by 96 publications

(22 citation statements)

References 40 publications

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“…A recent study demonstrated that serum TIMP-1 levels were significantly higher in patients with progressive RA over those who had radiographically stable disease [19]. These findings differed from previous studies, in which no association was observed between TIMP-1 levels and radiographic outcome [13,33,34]. In the context of our in vitro studies MMP-1, MMP-3 and TIMP-1 levels were elevated in response to IL-1β treatment.…”

Section: Discussioncontrasting

confidence: 95%

Interferon-γ inhibits interleukin-1β-induced matrix metalloproteinase production by synovial fibroblasts and protects articular cartilage in early arthritis

et al. 2010

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IntroductionThe first few months after symptom onset represents a pathologically distinct phase in rheumatoid arthritis (RA). We used relevant experimental models to define the pathological role of interferon-γ (IFN-γ) during early inflammatory arthritis.MethodsWe studied IFN-γ's capacity to modulate interleukin-1β (IL-1β) induced degenerative responses using RA fibroblast-like synoviocytes (FLS), a bovine articular cartilage explant (BACE)/RA-FLS co-culture model and an experimental inflammatory arthritis model (murine antigen-induced arthritis (AIA)).ResultsIFN-γ modulated IL-1β driven matrix metalloproteinases (MMP) synthesis resulting in the down-regulation of MMP-1 and MMP-3 production in vitro. IFN-γ did not affect IL-1β induced tissue inhibitor of metalloproteinase-1 (TIMP-1) production by RA FLS but skewed the MMP/TIMP-1 balance sufficiently to attenuate glycosaminoglycan-depletion in our BACE model. IFN-γ reduced IL-1β expression in the arthritic joint and prevented cartilage degeneration on Day 3 of AIA.ConclusionsEarly therapeutic intervention with IFN-γ may be critical to orchestrate tissue-protective responses during inflammatory arthritis.

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Section: Discussioncontrasting

confidence: 95%

Interferon-γ inhibits interleukin-1β-induced matrix metalloproteinase production by synovial fibroblasts and protects articular cartilage in early arthritis

et al. 2010

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“…In human studies, an elevated serum MMP-3 level has been observed in subjects with joint injury [23] and OA [24-26]; serum MMP-3 level may predict the rate of cartilage loss in an OA joint [27]. Interestingly, our results indicated that serum MMP-3 level decreased after intra-articular MMP-3 inhibitor treatment.…”

Section: Discussionmentioning

confidence: 53%

Matrix metalloproteinase-3 inhibitor retards treadmill running-induced cartilage degradation in rats

Zhan

Gao

et al. 2011

Arthritis Res Ther

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IntroductionThe effect of intra-articular injection of matrix metalloproteinase (MMP)-3 inhibitor was investigated in a rat model to understand the role of MMP-3 in cartilage degradation induced by excessive loading from running.MethodsA total of 24 male Wistar rats were randomly assigned into groups of sedentary control (SED), high-intensity running (HIR), HIR + low dosage of MMP-3 Inhibitor I (HIRI1), and HIR + high dosage of MMP-3 Inhibitor I (HIRI2). Rats in the HIR, HIRI1 and HIRI2 groups were intensively trained for six weeks on the treadmill. Those in HIRI1 and HIRI2 groups were provided bilateral intra-articular injections of 80 μL of 0.2 mM and 2 mM MMP-3 Inhibitor I in knee joints once a week, respectively. Blood samples were collected to measure serum MMP-3 level using ELISA. Femoral condyles were collected to observe cartilage characteristics by histochemistry, and MMP-3 as well as collagen II was measured by immunohistochemistry. In addition, cartilage samples were obtained to assess MMP-3 mRNA expression by RT-PCR.ResultsHistological examination showed osteoarthritic changes in rats after six weeks of high intensity running. In comparison to the SED group, significant decreases in glycosaminoglycans (GAG) and collagen content were found in the HIR group, which corresponded to significant increase in serum MMP-3 level, cartilage MMP-3 activity and gene expression. However, such a degradative process was considerably retarded by intra-articular injection of MMP-3 inhibitor at higher dosage. Statistical differences were found between the HIR and HIRI2 groups with regard to GAG and collagen II content, serum MMP-3 level, cartilage MMP-3 activity and gene expression.ConclusionsHigh-intensity running for six weeks may lead to cartilage degradation in a rat model. It was shown that the chrondroprotective effect was offered by the use of intra-articular injection of MMP-3 inhibitor. MMP-3 acts as the key mediator of this catabolic change under such mechanical condition. The results also showed that MMP-3 selective inhibitor may be an effective option for retarding such osteoarthritic changes.

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“…Экспери-ментальные данные свидетельствуют о том, что мРНК ММП1, 3 и 13 постоянно экспрессируются в суставном хряще [11]. Кроме того, ММП и продукты деградации аг-греканов присутствуют в синовиальной жидкости здоро-вых людей [12,13].…”

Section: таблицаunclassified

Pathogenesis of Osteoarthritis and Substantiation of the Use of Strontium Ranelate

Зайцева¹,

Алексеева²,

Насонов³

2014

rsp

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Serum levels of collagenase, stromelysin‐1, and timp‐1

Cited by 96 publications

References 40 publications

Interferon-γ inhibits interleukin-1β-induced matrix metalloproteinase production by synovial fibroblasts and protects articular cartilage in early arthritis

Interferon-γ inhibits interleukin-1β-induced matrix metalloproteinase production by synovial fibroblasts and protects articular cartilage in early arthritis

Matrix metalloproteinase-3 inhibitor retards treadmill running-induced cartilage degradation in rats

Pathogenesis of Osteoarthritis and Substantiation of the Use of Strontium Ranelate

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