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Article ; Online: ADAMTS-5 takes centre stage in new developments for aggrecanase inhibitors.

Fosang, A J

2015 Volume 23, Issue 8, Page(s) 1231–1232

MeSH term(s)	ADAM Proteins/immunology ; Animals ; Antibodies, Monoclonal/pharmacology ; Cartilage, Articular/pathology ; Humans ; Osteoarthritis/immunology
Chemical Substances	Antibodies, Monoclonal ; ADAM Proteins (EC 3.4.24.-)
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	1167809-4
ISSN	1522-9653 ; 1063-4584
ISSN (online)	1522-9653
ISSN	1063-4584
DOI	10.1016/j.joca.2015.05.023
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Article ; Online: Transparency Is the Key to Quality.

Fosang, Amanda J / Colbran, Roger J

The Journal of biological chemistry

2015 Volume 290, Issue 50, Page(s) 29692–29694

MeSH term(s)	Blotting, Western ; National Institutes of Health (U.S.) ; Peer Review, Research ; Reproducibility of Results ; Uncertainty ; United States
Language	English
Publishing date	2015-12-11
Publishing country	United States
Document type	Editorial
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.E115.000002
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Article ; Online: Identifying the human aggrecanase.

Fosang, A J / Rogerson, F M

Osteoarthritis and cartilage

2010 Volume 18, Issue 9, Page(s) 1109–1116

Abstract: It is clear that A Disintegrin And Metalloproteinase with ThromboSpondin motif (ADAMTS)-5 is the major aggrecanase in mouse cartilage, however it is not at all clear which enzyme is the major aggrecanase in human cartilage. Identifying the human ... ...

Abstract	It is clear that A Disintegrin And Metalloproteinase with ThromboSpondin motif (ADAMTS)-5 is the major aggrecanase in mouse cartilage, however it is not at all clear which enzyme is the major aggrecanase in human cartilage. Identifying the human aggrecanase is difficult because multiple, independent, molecular processes determine the final level of enzyme activity. As investigators, we have good methods for measuring changes in the expression of ADAMTS mRNA, and good methods for detecting aggrecanase activity, but no methods that distinguish the source of the activity. In between gene expression and enzyme action there are many processes that can potentially enhance or inhibit the final level of activity. In this editorial we discuss how each of these processes affects ADAMTS activity and argue that measuring any one process in isolation has little value in predicting overall ADAMTS activity in vivo.
MeSH term(s)	ADAM Proteins/genetics ; ADAM Proteins/metabolism ; ADAMTS4 Protein ; ADAMTS5 Protein ; Cartilage, Articular/enzymology ; Epigenesis, Genetic ; Gene Expression Regulation ; Humans ; Procollagen N-Endopeptidase/genetics ; Procollagen N-Endopeptidase/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	RNA, Messenger ; ADAM Proteins (EC 3.4.24.-) ; ADAMTS5 Protein (EC 3.4.24.-) ; ADAMTS5 protein, human (EC 3.4.24.-) ; Procollagen N-Endopeptidase (EC 3.4.24.14) ; ADAMTS4 Protein (EC 3.4.24.82)
Language	English
Publishing date	2010-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1167809-4
ISSN	1522-9653 ; 1063-4584
ISSN (online)	1522-9653
ISSN	1063-4584
DOI	10.1016/j.joca.2010.06.014
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Article ; Online: Emerging Frontiers in cartilage and chondrocyte biology.

Fosang, Amanda J / Beier, Frank

Best practice & research. Clinical rheumatology

2011 Volume 25, Issue 6, Page(s) 751–766

Abstract: Articular cartilage is a uniquely ordered tissue that is designed to resist compression and redistribute load, but is poorly equipped for self-repair. The chondrocyte is the only resident cell type, responsible for maintaining a specialised and extensive ...

Abstract	Articular cartilage is a uniquely ordered tissue that is designed to resist compression and redistribute load, but is poorly equipped for self-repair. The chondrocyte is the only resident cell type, responsible for maintaining a specialised and extensive matrix that is avascular and lacks innervation. These attributes, as well as the slow turnover rate of aggrecan and type II collagen in mature articular cartilage, present a considerable challenge to the tissue engineer. Similarly, those attempting to halt the progression of cartilage erosion must contend with these unusual characteristics. This review explores the gaps in our knowledge of cartilage biology and pathology, including what is known about the relative contribution of collagenases and aggrecanases to cartilage degradation, the need to regulate the chondrocytic phenotype and the putative role of chondrocyte hypertrophy in the pathogenesis of degenerative and rheumatic joint disease. Recent advances in cartilage tissue engineering are also reviewed.
MeSH term(s)	Cartilage, Articular/pathology ; Cartilage, Articular/physiology ; Chondrocytes/pathology ; Chondrocytes/physiology ; Collagenases/metabolism ; Endopeptidases/metabolism ; Humans ; Osteoarthritis/pathology ; Osteoarthritis/therapy ; Rheumatic Diseases/pathology ; Rheumatic Diseases/therapy ; Tissue Engineering
Chemical Substances	Endopeptidases (EC 3.4.-) ; Collagenases (EC 3.4.24.-) ; aggrecanase (EC 3.4.99.-)
Language	English
Publishing date	2011-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052323-3
ISSN	1532-1770 ; 1521-6942
ISSN (online)	1532-1770
ISSN	1521-6942
DOI	10.1016/j.berh.2011.11.010
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Article ; Online: Glucocorticoids influence versican and chondroitin sulphate proteoglycan levels in the fetal sheep lung.

McDougall, Annie R A / Fosang, Amanda J / Faggian, Jessica / Wallace, Megan J / Crossley, Kelly J / Cole, Timothy J / Hooper, Stuart B

Respiratory research

2018 Volume 19, Issue 1, Page(s) 155

Abstract: Background: Prenatal glucocorticoid treatment decreases alveolar tissue volumes and facilitates fetal lung maturation, however the mechanisms responsible are largely unknown. This study examines whether changes in versican levels or sulphation patterns ... ...

Abstract	Background: Prenatal glucocorticoid treatment decreases alveolar tissue volumes and facilitates fetal lung maturation, however the mechanisms responsible are largely unknown. This study examines whether changes in versican levels or sulphation patterns of chondroitin sulphate (CS) side chains, are associated with glucocorticoid-induced reductions in peri-alveolar tissue volumes. Methods: Lung tissue was collected from 1) fetal sheep at 131 ± 0.1 days gestational age (GA) infused with cortisol (122-131d GA) to prematurely induce a pre-parturient-like rise in circulating cortisol, 2) fetal sheep at 143d GA bilaterally adrenalectomised (ADX) at 112d GA to remove endogenous cortisol and 3) fetal sheep at 124d GA in which bolus doses (2 × 11.4 mg) of betamethasone were administered to the pregnant ewe. The level and distribution of versican and CS glycosaminoglycans (GAG) were determined using immunohistochemistry (IHC). Fluorophore assisted carbohydrate electrophoresis (FACE) was used to determine changes in CS sulphation patterns. Results: Cortisol infusion significantly decreased chondrotin-6-sulphate levels (C-6-S) to 16.4 ± 0.7 AU, compared with saline-infused fetuses (18.9 ± 0.7 AU: p = 0.04) but did not significantly alter the level of versican or chondroitin-4-sulphate (C-4-S). ADX significantly increased the level of C-4-S (28.2 ± 2.2 AU), compared with sham-operated fetuses (17.8 ± 2.0 AU; p = 0.006) without altering versican or C-6-S levels. Betamethasone significantly decreased versican, C-4-S and C-6-S in the fetal sheep lung (19.2 ± 0.9 AU, 24.9 ± 1.4 AU and 23.2 ± 1.0 AU, respectively), compared with saline-exposed fetuses (24.3 ± 0.4 AU, p = 0.0004; 33.3±0.6 AU, p = 0.0003; 29.8±1.3 AU, 0.03, respectively). Conclusions: These results indicate that glucocorticoids alter versican levels and CS side chain microstructure in alveolar lung tissue. Betamethasone appears to have a greater impact on versican and CS side chains than cortisol.
MeSH term(s)	Animals ; Chondroitin Sulfates/biosynthesis ; Female ; Fetal Development/drug effects ; Fetal Development/physiology ; Fetus ; Glucocorticoids/pharmacology ; Lung/drug effects ; Lung/growth & development ; Lung/metabolism ; Pregnancy ; Proteoglycans/biosynthesis ; Sheep ; Versicans/biosynthesis
Chemical Substances	Glucocorticoids ; Proteoglycans ; Versicans (126968-45-4) ; Chondroitin Sulfates (9007-28-7)
Language	English
Publishing date	2018-08-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/s12931-018-0854-4
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Article ; Online: Is cartilage matrix breakdown an appropriate therapeutic target in osteoarthritis--insights from studies of aggrecan and collagen proteolysis?

Little, Christopher B / Fosang, Amanda J

Current drug targets

2010 Volume 11, Issue 5, Page(s) 561–575

Abstract: Progressive cartilage degradation is considered a hallmark of osteoarthritis (OA), and as such methods to inhibit this process have been extensively investigated as potential disease-modifying therapies. However, all tissues of the joint are affected by ... ...

Abstract	Progressive cartilage degradation is considered a hallmark of osteoarthritis (OA), and as such methods to inhibit this process have been extensively investigated as potential disease-modifying therapies. However, all tissues of the joint are affected by disease in OA, and it is likely that the pain and disability which are the major clinical symptoms of OA, arise predominantly from pathology in these extra-cartilaginous structures. It is unclear therefore, whether specifically targeting inhibition of cartilage matrix breakdown will ameliorate global joint pathology and thereby affect the clinically-relevant OA-related disability. We have investigated this question by reviewing the literature and data available from studies of genetically-modified (GM) mice. A total of 79 different GM strains were identified in which OA-like cartilage erosion was analysed, 53 with increased, 18 with no change, and 8 with decreased cartilage damage. Inhibition of OA cartilage damage was afforded by mutations that either reduced chondrocyte hypertrophy or abrogated proteolysis of aggrecan and collagen II in cartilage. There was an association between increased cartilage breakdown and changes in subchondral bone, osteophytosis and synovial hyperplasia in GM mice. However, the effect of significantly inhibiting cartilage damage on pathology in other joints tissues has been less well examined. There appeared to be no diminution of osteophyte development in chondroprotected GM mice strains, but a possible reduction in subchondral bone plate changes. To date, there is no conclusive data on the effect of inhibiting cartilage breakdown on clinical signs of OA in GM mice. These studies have highlighted the tremendous advances studies of GM mice have afforded us in understanding the pathophysiology of cartilage degradation in OA. Furthermore they demonstrate the feasibility of targeting cartilage matrix destruction. However, it is evident that an important direction for ongoing research will be to determine the effect of successful protection of cartilage structural integrity on pathology in other tissues in the OA joint, and the clinical signs of the disease.
MeSH term(s)	Aggrecans/metabolism ; Animals ; Arthritis, Experimental/drug therapy ; Arthritis, Experimental/genetics ; Arthritis, Experimental/metabolism ; Cartilage/metabolism ; Cartilage/pathology ; Cartilage Oligomeric Matrix Protein ; Collagen Type II/metabolism ; Drug Delivery Systems/methods ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Glycoproteins/genetics ; Glycoproteins/metabolism ; Humans ; Matrilin Proteins ; Mice ; Mice, Transgenic ; Models, Biological ; Osteoarthritis/drug therapy ; Osteoarthritis/genetics ; Osteoarthritis/metabolism ; Protease Inhibitors/therapeutic use ; Species Specificity
Chemical Substances	Aggrecans ; Cartilage Oligomeric Matrix Protein ; Collagen Type II ; Extracellular Matrix Proteins ; Glycoproteins ; Matn1 protein, mouse ; Matrilin Proteins ; Protease Inhibitors ; TSP5 protein, human
Language	English
Publishing date	2010-03-02
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	2064859-5
ISSN	1873-5592 ; 1389-4501
ISSN (online)	1873-5592
ISSN	1389-4501
DOI	10.2174/138945010791011956
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Article ; Online: ADAMTS-9 in Mouse Cartilage Has Aggrecanase Activity That Is Distinct from ADAMTS-4 and ADAMTS-5.

Rogerson, Fraser M / Last, Karena / Golub, Suzanne B / Gauci, Stephanie J / Stanton, Heather / Bell, Katrina M / Fosang, Amanda J

International journal of molecular sciences

2019 Volume 20, Issue 3

Abstract: A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 and ADAMTS-5 are the principal aggrecanases in mice and humans; however, mice lacking the catalytic domain of both enzymes (TS-4/5∆cat) have no skeletal phenotype, suggesting there ...

Abstract	A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 and ADAMTS-5 are the principal aggrecanases in mice and humans; however, mice lacking the catalytic domain of both enzymes (TS-4/5∆cat) have no skeletal phenotype, suggesting there is an alternative aggrecanase for modulating normal growth and development in these mice. We previously identified aggrecanase activity that (a) cleaved at E↓G rather than E↓A bonds in the aggrecan core protein, and (b) was upregulated by retinoic acid but not IL-1α. The present study aimed to identify the alternative aggrecanase. Femoral head cartilage explants from TS-4/5∆cat mice were stimulated with IL-1α or retinoic acid and total RNA was analysed by microarray. In addition to ADAMTS-5 and matrix metalloproteinase (MMP)-13, which are not candidates for the novel aggrecanase, the microarray analyses identified MMP-11, calpain-5 and ADAMTS-9 as candidate aggrecanases upregulated by retinoic acid. When calpain-5 and MMP-11 failed to meet subsequent criteria, ADAMTS-9 emerged as the most likely candidate for the novel aggrecanase. Immunohistochemistry revealed ADAMTS-9 expression throughout the mouse growth plate and strong expression, particularly in the proliferative zone of the TS-4/5-∆cat mice. In conclusion, ADAMTS-9 has a novel specificity for aggrecan, cleaving primarily at E↓G rather than E↓A bonds in mouse cartilage. ADAMTS-9 might have more important roles in normal skeletal development compared with ADAMTS-4 and ADAMTS-5, which have key roles in joint pathology.
MeSH term(s)	ADAMTS4 Protein/metabolism ; ADAMTS5 Protein/metabolism ; ADAMTS9 Protein/genetics ; ADAMTS9 Protein/metabolism ; Aggrecans/metabolism ; Animals ; Arthritis/genetics ; Arthritis/metabolism ; Cartilage/metabolism ; Cells, Cultured ; Endopeptidases/metabolism ; Immunohistochemistry ; Matrix Metalloproteinase 13/genetics ; Matrix Metalloproteinase 13/metabolism ; Mice ; RNA, Messenger/metabolism
Chemical Substances	Aggrecans ; RNA, Messenger ; Endopeptidases (EC 3.4.-) ; ADAMTS5 Protein (EC 3.4.24.-) ; ADAMTS9 Protein (EC 3.4.24.-) ; Matrix Metalloproteinase 13 (EC 3.4.24.-) ; ADAMTS4 Protein (EC 3.4.24.82) ; aggrecanase (EC 3.4.99.-)
Language	English
Publishing date	2019-01-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20030573
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Article ; Online: Abundant LacZ activity in the absence of Cre expression in the normal and inflamed synovium of adult Col2a1-Cre; ROSA26RLacZ reporter mice.

Fosang, A J / Golub, S B / East, C J / Rogerson, F M

Osteoarthritis and cartilage

2013 Volume 21, Issue 2, Page(s) 401–404

Abstract: Recent analyses of Col2a1-Cre; ROSA26R reporter mice showed that synovial fibroblasts in 7-day mice were LacZ positive, due to a history of Col2a1-Cre expression conferred by their origin in the interzone of the developing joint. We have examined LacZ ... ...

Abstract	Recent analyses of Col2a1-Cre; ROSA26R reporter mice showed that synovial fibroblasts in 7-day mice were LacZ positive, due to a history of Col2a1-Cre expression conferred by their origin in the interzone of the developing joint. We have examined LacZ staining in adult Col2a1-Cre(+/0); ROSA26R(LacZ) mice, with and without inflammatory arthritis, and found that synovial fibroblasts in normal and inflamed synovium are LacZ positive, but Cre negative. Our results suggest that Cre-mediated recombination in joint interzone cells during development endure in adult synovial cells despite the absence of ongoing Cre expression. These findings have important implications and applications for the study of synovial inflammation in models of experimental arthritis.
MeSH term(s)	Animals ; Arthritis/pathology ; Arthritis/physiopathology ; Collagen Type II/genetics ; Collagen Type II/physiology ; Disease Models, Animal ; Fibroblasts/pathology ; Fibroblasts/physiology ; Gene Expression Regulation/physiology ; Genes, Reporter/genetics ; Genes, Reporter/physiology ; Integrases/deficiency ; Integrases/genetics ; Integrases/physiology ; Knee Joint ; Lac Operon/genetics ; Lac Operon/physiology ; Mice ; Mice, Transgenic ; Proteins/genetics ; Proteins/physiology ; RNA, Untranslated ; Synovial Membrane/pathology ; Synovial Membrane/physiopathology ; Time Factors
Chemical Substances	Col2a1 protein, mouse ; Collagen Type II ; Gt(ROSA)26Sor non-coding RNA, mouse ; Proteins ; RNA, Untranslated ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2013-02
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1167809-4
ISSN	1522-9653 ; 1063-4584
ISSN (online)	1522-9653
ISSN	1063-4584
DOI	10.1016/j.joca.2012.11.013
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Article ; Online: Drug insight: aggrecanases as therapeutic targets for osteoarthritis.

Fosang, Amanda J / Little, Christopher B

Nature clinical practice. Rheumatology

2008 Volume 4, Issue 8, Page(s) 420–427

Abstract: In healthy cartilage, effective weight-bearing requires a high concentration of intact aggrecan. Degradation and loss of aggrecan are features of osteoarthritis (OA). It is unclear whether ADAMTS-4, ADAMTS-5, or both of these aggrecanases from the ADAMTS ...

Abstract	In healthy cartilage, effective weight-bearing requires a high concentration of intact aggrecan. Degradation and loss of aggrecan are features of osteoarthritis (OA). It is unclear whether ADAMTS-4, ADAMTS-5, or both of these aggrecanases from the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) enzyme family, are responsible for aggrecanolysis in human OA, and at what stage of disease these enzymes are active. Several potential disease-modifying agents for OA include glucosamine and chondroitin sulfate, diacerhein, and pentosan polysulfate; although their mechanisms of action in vivo are unknown, data from in vitro studies and animal models suggest that their efficacy might be partly due to inhibition of proinflammatory pathways that lead to downregulation of ADAMTS enzymes. Some histone deacetylase inhibitors that are successfully used to treat cancer can block ADAMTS-5 expression; however, these inhibitors will only be considered as potential therapies for OA if their toxicity is markedly reduced. ADAMTS inhibitors currently in development are expected to show excellent specificity now that crystal structures for several ADAMTS enzymes are available to guide drug design. ADAMTS-4 and ADAMTS-5 are appropriate targets for OA therapies, but ultimately, inhibitors of these enzymes will form only part of a larger arsenal of therapies.
MeSH term(s)	ADAM Proteins/antagonists & inhibitors ; ADAMTS4 Protein ; ADAMTS5 Protein ; Aggrecans/metabolism ; Animals ; Humans ; Isoenzymes ; Osteoarthritis/drug therapy ; Osteoarthritis/enzymology ; Osteoarthritis/etiology ; Procollagen N-Endopeptidase/antagonists & inhibitors
Chemical Substances	Aggrecans ; Isoenzymes ; ADAM Proteins (EC 3.4.24.-) ; ADAMTS5 Protein (EC 3.4.24.-) ; ADAMTS5 protein, human (EC 3.4.24.-) ; Procollagen N-Endopeptidase (EC 3.4.24.14) ; ADAMTS4 Protein (EC 3.4.24.82) ; ADAMTS4 protein, human (EC 3.4.24.82)
Language	English
Publishing date	2008-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2228569-6
ISSN	1745-8390 ; 1745-8382
ISSN (online)	1745-8390
ISSN	1745-8382
DOI	10.1038/ncprheum0841
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Article ; Online: Disrupted type II collagenolysis impairs angiogenesis, delays endochondral ossification and initiates aberrant ossification in mouse limbs.

Gauci, S J / Golub, S B / Tatarczuch, L / Lee, E / Chan, D / Walsh, N C / Little, C B / Stanton, H / Lokmic, Z / Sims, N A / Mackie, E J / Fosang, A J

Matrix biology : journal of the International Society for Matrix Biology

2019 Volume 83, Page(s) 77–96

Abstract: Cartilage remodelling and chondrocyte differentiation are tightly linked to angiogenesis during bone development and endochondral ossification. To investigate whether collagenase-mediated cleavage of the major cartilage collagen (collagen II) plays a ... ...

Abstract	Cartilage remodelling and chondrocyte differentiation are tightly linked to angiogenesis during bone development and endochondral ossification. To investigate whether collagenase-mediated cleavage of the major cartilage collagen (collagen II) plays a role in this process, we generated a knockin mouse in which the mandatory collagenase cleavage site at PQG
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Chondrocytes/cytology ; Collagen Type II/chemistry ; Collagen Type II/genetics ; Collagen Type II/metabolism ; Collagenases/metabolism ; Female ; Gene Knock-In Techniques ; Growth Plate/abnormalities ; Growth Plate/blood supply ; Male ; Mice ; Neovascularization, Physiologic ; Osteogenesis
Chemical Substances	Col2a1 protein, mouse ; Collagen Type II ; Collagenases (EC 3.4.24.-)
Language	English
Publishing date	2019-08-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1183793-7
ISSN	1569-1802 ; 0945-053X
ISSN (online)	1569-1802
ISSN	0945-053X
DOI	10.1016/j.matbio.2019.08.001
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