Stimulation of 92‐kd gelatinase (matrix metalloproteinase 9) production by interleukin‐17 in human monocyte/macrophages: A possible role in rheumatoid arthritis

Jovanović, Dragan; Martel‐Pelletier, Johanne; Battista, John A. Di; Mineau, François; Jolicoeur, F C; Benderdour, Mohamed; Pelletier, Jean‐Pierre

doi:10.1002/1529-0131(200005)43:5<1134::aid-anr24>3.0.co;2-#

Cited by 161 publications

(100 citation statements)

References 58 publications

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“…Many studies have shown the importance of IL-1 in cartilage metabolism and in the regulation of these genes (33)(34)(35), although IL-17 also influences the expression of these genes. IL-17 increases the spontaneous production of MMP-1 by synoviocytes (36) and induces MMP-9 production in human monocyte/macrophages (15). In IL-17-treated chondrocytes, expression of mRNA for MMPs 1, 3, and 13 was detected, and a synergistic induction of these MMPs was seen when IL-17 was combined with other proinflammatory cytokines (14).…”

Section: Discussionmentioning

confidence: 99%

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Induction of cartilage damage by overexpression of T cell interleukin‐17A in experimental arthritis in mice deficient in interleukin‐1

Koenders¹,

Lubberts²,

Oppers‐Walgreen³

et al. 2005

Arthritis & Rheumatism

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Objective. To examine the capacity of T cell interleukin-17A (IL-17A; referred to hereinafter as IL-17) to induce cartilage damage during experimental arthritis in the absence of IL-1.Methods. Local IL-17 gene transfer was performed in the knee joint of IL-1-deficient mice and wild-type controls during streptococcal cell wall (SCW)-induced arthritis. Knee joints were isolated at various time points for histologic analysis of cartilage proteoglycan (PG) depletion. Expression of messenger RNA for inducible nitric oxide synthase, matrix metalloproteinases (MMPs) 3, 9, and 13, and ADAMTS-4 was determined by quantitative polymerase chain reaction analysis. VDIPEN staining was analyzed to study MMPmediated cartilage damage. In addition, systemic anti-IL-1␣/␤ antibody treatment was performed in mice immunized with type II collagen and injected locally with an adenoviral vector expressing IL-17 or with control adenovirus. Knee joints were isolated and analyzed for cartilage PG depletion, chondrocyte death, and cartilage surface erosion. Conclusion. These data show the capacity of IL-17 to replace the catabolic function of IL-1 in cartilage damage during experimental arthritis. Results. During SCW-induced arthritis

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Section: Discussionmentioning

confidence: 99%

“…independently of IL-1 (11), and IL-17-induced production of matrix metalloproteinase 9 (MMP-9) in human monocytes and macrophages is not inhibited by IL-1 receptor antagonist (IL-1Ra) (15).…”

mentioning

confidence: 99%

Induction of cartilage damage by overexpression of T cell interleukin‐17A in experimental arthritis in mice deficient in interleukin‐1

Koenders¹,

Lubberts²,

Oppers‐Walgreen³

et al. 2005

Arthritis & Rheumatism

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“…MMP-9 plays a critical role in the invasion of the synovial tissue, leading to cartilage destruction and bone erosion in RA (7,10,33,34). The importance of this enzyme in arthritis is highlighted by the finding that MMP-9-knockout mice display less severe antibodyinduced arthritis than do wild-type mice (10).…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of matrix metalloproteinase 2 and matrix metalloproteinase 9 by activated protein C: Relevance to inflammation in rheumatoid arthritis

Xue

March

Sambrook

2007

Arthritis & Rheumatism

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Objective. To investigate the in vitro effect of activated protein C (APC), a natural anticoagulant and novel antiinflammatory agent, on the regulation of the gelatinases matrix metalloproteinase 2 (MMP-2) and MMP-9.Methods. Synovial fibroblasts and peripheral blood monocytes isolated from patients with rheumatoid arthritis (RA) or osteoarthritis (OA) and Mono Mac6 cells were used in this study. After treatment, cells and culture supernatants were collected for zymography, enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blot analysis.Results. Fibroblasts and monocytes from RA patients produced substantially more MMP-9 than did those from OA patients; however, there was no difference in MMP-2 production. The addition of recombinant APC markedly reduced MMP-9 at the gene and protein levels. In contrast, APC up-regulated and activated MMP-2. Using a blocking antibody to the endothelial protein C receptor (EPCR), we showed that the inhibition of MMP-9 by APC was EPCR-dependent. Furthermore, APC directly suppressed the production of tumor necrosis factor (TNF) and the activation of NF-B and MAP kinase p38, and inhibitors of NF-B or p38 reduced the production of MMP-9, suggesting that APC inhibits MMP-9 by blocking TNF, NF-B, and p38. Thus, APC acts on MMP-9 by binding to EPCRs on the cell surface and, subsequently, inhibiting the intracellular activation of the proinflammatory signaling molecules NF-B and p38.Conclusion. APC appears to be the first physiologic agent to inhibit the production of proinflammatory MMP-9, yet increase antiinflammatory MMP-2 activity.

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“…IL-17A may contribute to asthma pathogenesis through a number of different mechanisms such as induction of neutrophilia and stimulation of lung innate and structural cells to secrete proinflammatory cytokines (15,43,44). Also worthy of note is the association of IL-17A with subepithelial fibrosis, a feature of airway remodelling shown in some studies to correlate with asthma severity (45).…”

Section: Nanzer Et Al 15mentioning

confidence: 99%

Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion

Nanzer

Chambers

Ryanna

et al. 2013

Journal of Allergy and Clinical Immunology

161

144

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Stimulation of 92‐kd gelatinase (matrix metalloproteinase 9) production by interleukin‐17 in human monocyte/macrophages: A possible role in rheumatoid arthritis

Abstract: IL-17 may contribute to an unbalanced production of proinflammatory cytokines and MMP-9 in diseased articular joint tissues by interacting with the macrophages in the rheumatoid synovium.

Cited by 161 publications

References 58 publications

Induction of cartilage damage by overexpression of T cell interleukin‐17A in experimental arthritis in mice deficient in interleukin‐1

Induction of cartilage damage by overexpression of T cell interleukin‐17A in experimental arthritis in mice deficient in interleukin‐1

Differential regulation of matrix metalloproteinase 2 and matrix metalloproteinase 9 by activated protein C: Relevance to inflammation in rheumatoid arthritis

Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion

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