Interleukin-17F affects cartilage matrix turnover by increasing the expression of collagenases and stromelysin-1 and by decreasing the expression of their inhibitors and extracellular matrix components in chondrocytes

Tanigawa, Shihoko; Aida, Yasuhiro; Kawato, Takayuki; Honda, Kazuo; Nakayama, Go; Motohashi, Masafumi; Suzuki, Naoto; Ochiai, Kuniyasu; Matsumura, Hideo; Maeno, Masao

doi:10.1016/j.cyto.2011.08.015

Cited by 25 publications

(17 citation statements)

References 37 publications

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“…In addition to its anti-inflammatory effects in binding fragments of hyaluronan, the hyaluronan-binding domain is known to be involved in extracellular matrix stability [39]. Interesting, a recent study reported that IL-17F, sharing high homology with other IL-17 family members including IL-17A, can regulate extracellular matrix stability and stimulate cartilage degradation by increasing the expression of collagenases (matrix metalloproteinase (MMP)-1 and -13) and stromelysin-1 (MMP-3) and by decreasing the expression of their inhibitors (tissue inhibitor of metalloproteinase-2 and -4), type II collagen, aggrecan and link protein in chondrocytes [40]. It is believed that defective biosynthesis and/or degradation of the extracellular matrix has the potential to alter the morphologic and functional characteristics of Bruch's membrane, an initial site of pathological change during AMD development.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory recombinant TSG-6 stabilizes the progression of focal retinal degeneration in a murine model

Tuo

Cao

Shen

et al. 2012

J Neuroinflammation

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Background Inflammatory responses are detected in the retina of patients with age-related macular degeneration and Ccl2 -/- /Cx3cr1 -/- mice on rd8 background,( Ccl2 -/- /Cx3cr1 -/- mice) a model that develops progressive age-related macular degeneration-like retinal lesions including focal photoreceptor degeneration, abnormal retinal pigment epithelium and A2E accumulation. Tumor necrosis factor-inducible gene 6 protein is an anti-inflammatory protein and has been shown to improve myocardial infarction outcome and chemically injured cornea in mice by suppressing inflammation. In this study, we evaluated the effect of an intravitreous injection of recombinant TSG-6 on the retinal lesions of Ccl2 -/- /Cx3cr1 -/- mice. Methods Recombinant TSG-6 (400 ng) was administered by intravitreous injection into the right eye of six-week-old C cl2 -/- /Cx3cr1 -/- mice. Their left eye was injected with phosphate-buffered saline as a control. Funduscopic pictures were taken before injection and sequentially once a month after injection. The mice were killed two months after injection and the ocular histology examined. Retinal A2E, a major component of lipofuscin, was measured by high performance liquid chromatography. The microarray of ocular mRNA of 92 immunological genes was performed. The genes showing differentiated expression in microarray were further compared between the injected right eye and the contralateral (control) eye by [real-time quantitative reverse transcription polymerase chain reaction] qRT-PCR. Results The continuous monitoring of the fundus for two months showed a slower progression or alleviation of retinal lesions in the treated right eyes as compared with the untreated left eyes. Among 23 pairs of eyes, the lesion levels improved in 78.3%, stayed the same in 8.7% and progressed in 13.0%. Histology confirmed the clinical observation. Even though there was no difference in the level of A2E between the treated and the untreated eyes, microarray analysis of 92 immune genes showed that IL-17a was substantially decreased after the treatment. Expression of TNF-α showed a similar pattern to IL-17a . The results were consistent in duplicated arrays and confirmed by qRT-PCR. Conclusions We concluded that intravitreous administration of recombinant TSG-6 might stabilize retinal lesions in Ccl2 -/- /Cx3cr1 -/- mice on rd8 background. Modulation of ocular immunological gene expressions, especially IL-17a, could be one of the mechanisms.

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory recombinant TSG-6 stabilizes the progression of focal retinal degeneration in a murine model

Tuo

Cao

Shen

et al. 2012

J Neuroinflammation

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“…In mouse models, miR‐29b expression peaks in the days following destabilization of the medial meniscus surgery, but decreases gradually with advancing OA to reach equivalent levels to controls within 6 weeks 32,55 . How miR‐29s contribute to cartilage destruction in OA is unclear but their involvement may be linked to the actions of proinflammatory cytokines, such as interleukin‐1 β (IL‐1β) and tumor necrosis factor alpha (TNF‐α), that are released from the synovium and chondrocytes during OA pathogenesis 59,60 . IL‐1β has been reported to increase or decrease the expression of miR‐29b in human OA chondrocytes in culture whereas IL‐1β stimulation of the chondrosarcoma SW1353 cell line has no effect on miR‐29b expression 32,61,62 .…”

Section: Role Of Mir‐29 Family In Osteoarthritismentioning

confidence: 99%

The role of miR‐29 family in disease

Horita

Farquharson

Stephen

2021

J of Cellular Biochemistry

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MicroRNAs are small noncoding RNAs that can bind to the target sites in the 3’‐untranslated region of messenger RNA to regulate posttranscriptional gene expression. Increasing evidence has identified the miR‐29 family, consisting of miR‐29a, miR‐29b‐1, miR‐29b‐2, and miR‐29c, as key regulators of a number of biological processes. Moreover, their abnormal expression contributes to the etiology of numerous diseases. In the current review, we aimed to summarize the differential expression patterns and functional roles of the miR‐29 family in the etiology of diseases including osteoarthritis, osteoporosis, cardiorenal, and immune disease. Furthermore, we highlight the therapeutic potential of targeting members of miR‐29 family in these diseases. We present miR‐29s as promoters of osteoblast differentiation and apoptosis but suppressors of chondrogenic and osteoclast differentiation, fibrosis, and T cell differentiation, with clear avenues for therapeutic manipulation. Further research will be crucial to identify the precise mechanism of miR‐29 family in these diseases and their full potential in therapeutics.

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“…Moreover, IL-17A inhibits proteoglycan synthesis, enhances NO production, and acts in synergy with TNF-alpha in the destruction of the cartilage matrix [47–49]. Other studies suggest that IL-17F stimulates cartilage degradation by increasing the expression of collagenases (MMP-1 and MMP-13) and stromelysin-1 (MMP-3) and by decreasing the expression of their inhibitors (TIMP-2 and TIMP-4) or ECM components (type II collagen, aggrecan) [50]. Furthermore, IL-17A stimulates the release of a few chemokines (CXCL1, IL-8, and CCL2) by human chondrocytes, which also induces the secretion of MMPs or iNOS.…”

Section: Role Of Il-17a In Cartilage and Joint Biologymentioning

confidence: 99%

Implication of IL-17 in Bone Loss and Structural Damage in Inflammatory Rheumatic Diseases

Goff

Bouvard

Lequerré

et al. 2019

Mediators of Inflammation

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Proinflammatory cytokines play an important role in the systemic and focal bone loss associated with chronic inflammatory diseases. Targeting these cytokines with biologics and small molecules has led to a major improvement of the bone health of patients with inflammatory arthritis. Cytokines from the IL-17 family have been shown to be involved in the pathogenesis of several diseases such as spondyloarthritis, psoriatic arthritis, or psoriasis. IL-17A has been the first described and the most studied. The recent development of targeted therapies against IL-17A or its receptor and their efficacy has confirmed the importance of this cytokine in the development of inflammatory diseases. The aim of this review was to describe the effects of the IL-17 family and more particularly of IL-17A on bone and cartilage tissues. At the cellular level, IL-17A is proosteoclastogenic whereas its effects on osteoblasts depend on the stage of differentiation of these cells. In vivo, IL-17A is not required for normal bone homeostasis but plays an important role in bone loss notably in an ovariectomized mouse model of osteoporosis. Preliminary data from clinical trials showed a stabilisation of bone density in patients treated with anti-IL-17A antibodies. IL-17A plays a central role in the cartilage damage through the induction of collagenases and by decreasing the expression of their inhibitors in synergy with the other proinflammatory cytokines. The prevention of structural damage by anti-IL-17A therapies has been demonstrated in several pivotal clinical trials. Overall, blocking the IL-17A pathway seems to have a positive effect on the bone and cartilage damage observed in inflammatory arthritis. Differences and specificity of these effects compared to those already described with other biologics such as anti-TNF therapies remain to be explored.

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Interleukin-17F affects cartilage matrix turnover by increasing the expression of collagenases and stromelysin-1 and by decreasing the expression of their inhibitors and extracellular matrix components in chondrocytes

Cited by 25 publications

References 37 publications

Anti-inflammatory recombinant TSG-6 stabilizes the progression of focal retinal degeneration in a murine model

Anti-inflammatory recombinant TSG-6 stabilizes the progression of focal retinal degeneration in a murine model

The role of miR‐29 family in disease

Implication of IL-17 in Bone Loss and Structural Damage in Inflammatory Rheumatic Diseases

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