Microscopic localization of active gelatinases in equine osteochondritis dissecans (OCD) cartilage

Al-Hizab, F. A.; Clegg, Peter; Thompson, Catherine C.; Carter, Stuart

doi:10.1053/joca.2002.0811

Cited by 25 publications

(20 citation statements)

References 40 publications

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“…41 We examined the gene expression levels of gelatinases and their endogenous inhibitors, the TIMPs. In co-cultured chondrocytes, we found that IL-1β-regulated MMPs and TIMPs at the transcriptional level (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

The effects of interleukin-1β in modulating osteoclast-conditioned medium’s influence on gelatinases in chondrocytes through mitogen-activated protein kinases

Xie

Cai

et al. 2015

Int J Oral Sci

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Osteoarthritis is recognised to be an interactive pathological process involving the cartilage, subchondral bone and synovium. The signals from the synovium play an important role in cartilage metabolism, but little is known regarding the influence of the signalling from bone. Additionally, the collagenases and stromelysin-1 are involved in cartilage catabolism through mitogen-activated protein kinase (MAPK) signalling, but the role of the gelatinases has not been elucidated. Here, we studied the influence of osteoclastic signals on chondrocytes by characterising the expression of interleukin-1β (IL-1β)-induced gelatinases through MAPK signalling. We found that osteoclast-conditioned media attenuated the gelatinase activity in chondrocytes. However, IL-1β induced increased levels of gelatinase activity in the conditioned media group relative to the mono-cultured chondrocyte group. More specifically, IL-1β restored high levels of gelatinase activity in c-Jun N-terminal kinase inhibitor-pretreated chondrocytes in the conditioned media group and led to lower levels of gelatinase activity in extracellular signal-regulated kinase or p38 inhibitor-pretreated chondrocytes. Gene expression generally correlated with protein expression. Taken together, these results show for the first time that signals from osteoclasts can influence gelatinase activity in chondrocytes. Furthermore, these data show that IL-1β restores gelatinase activity through MAPK inhibitors; this information can help to increase the understanding of the gelatinase modulation in articular cartilage.

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Section: Discussionmentioning

confidence: 99%

The effects of interleukin-1β in modulating osteoclast-conditioned medium’s influence on gelatinases in chondrocytes through mitogen-activated protein kinases

Xie

Cai

et al. 2015

Int J Oral Sci

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“…MMP-2 (also known as gelatinase A) can degrade type IV collagen of basement membranes, collagen types V, VII, and X, as well as denatured collagen (gelatin), fibronectin, laminin, elastin, and proteoglygans [52]. MMP-2 activity also is increased in joint disease in the horse, [38,53] and dog [54]. Furthermore, MMP-2 activation has been identified in a variety of joint diseases [55].…”

Section: Discussionmentioning

confidence: 99%

“…In the arthritides (including OA and rheumatoid arthritis [RA]), this balance is disrupted, leading to a net loss of articular cartilage. Evidence of altered proteinase activity also has been identified in OC tissue [38][39][40].…”

Section: Introductionmentioning

confidence: 89%

MT3-MMP (MMP-16) is Downregulated byIn VitroCytokine Stimulation of Cartilage, but Unaltered in Naturally Occurring Equine Osteoarthritis and Osteochondrosis

Garvican

Vaughan-Thomas

Redmond

et al. 2008

Connective Tissue Research

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Matrix degradation by metalloproteinases is considered a key feature in the loss of articular cartilage seen in many joint diseases. Membrane-type matrix metalloproteinase-3 (MT3-MMP) expression is elevated in human cartilage in end-stage osteoarthritis. We investigated whether MT3-MMP is similarly regulated in cartilage in two naturally occurring arthropathies in vivo and whether proinflammatory cytokines regulate its expression in vitro. MT3-MMP expression was evaluated in cartilage from horses with osteoarthritis and osteochondrosis and compared with age- and site-matched normal cartilage. MT3-MMP also was measured in normal cartilage stimulated with proinflammatory cytokines. MT3-MMP expression was not significantly altered in either osteoarthritis or osteochondrosis cartilage. However, gene expression was significantly downregulated by the addition of recombinant human interleukin-1beta, oncostatin M, or tumor necrosis factor-alpha to normal cartilage explants. The results suggest that MT3-MMP may not have a role in matrix destruction in equine cartilage diseases. Further work is required to characterize its regulation and function.

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“…In recent years, many investigators have focused their research on the biochemical events involved in the pathogenesis of joint diseases, but few studies have addressed the aetiology of OCD. Some authors have reported an increase in the catabolic activity of chondrocytes with enzymatic degradation of the extracellular matrix due to the action of metalloproteinases, 5 but further studies aimed at elucidating the mechanisms involved are needed. Apoptosis has been identified as one of the mechanisms associated with different processes observed in osteoarthritis (OA) and rheumatoid arthritis 6 .…”

mentioning

confidence: 99%

Osteochondritis dissecans

et al. 2007

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Microscopic localization of active gelatinases in equine osteochondritis dissecans (OCD) cartilage

Cited by 25 publications

References 40 publications

The effects of interleukin-1β in modulating osteoclast-conditioned medium’s influence on gelatinases in chondrocytes through mitogen-activated protein kinases

The effects of interleukin-1β in modulating osteoclast-conditioned medium’s influence on gelatinases in chondrocytes through mitogen-activated protein kinases

MT3-MMP (MMP-16) is Downregulated byIn VitroCytokine Stimulation of Cartilage, but Unaltered in Naturally Occurring Equine Osteoarthritis and Osteochondrosis

Osteochondritis dissecans

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