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Cited by 489

The DOI matches its Crossref record; 194 of the 194 references it cites were found in a registry or an index.

Roles of inflammatory and anabolic cytokines in cartilage metabolism: signals and multiple effectors converge upon MMP-13 regulation in osteoarthritis

Open access
535 East 70th Street, Caspary Research Building, 5th Floor, New York, NY 10021, USA, Goldring, MB, Otero, M, Plumb, DA, Dragomir, C, Favero, M, EI Hachem, K, Hashimoto, K, Roach, HI, Olivotto, E, Borzì, RM, Marcu, KB·2011·European Cells and Materials
DOI 10.22203/ecm.v021a16
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Abstract

Human cartilage is a complex tissue of matrix proteins that vary in amount and orientation from superficial to deep layers and from loaded to unloaded zones. A major challenge to efforts to repair cartilage by stem cell-based and other tissue engineering strategies is the inability of the resident chondrocytes to lay down new matrix with the same structural and resilient properties that it had upon its original formation. This is particularly true of the collagen network, which is susceptible to cleavage once proteoglycans are depleted. Thus, a thorough understanding of the similarities and particularly the marked differences in mechanisms of cartilage remodeling during development, osteoarthritis, and aging may lead to more effective strategies for preventing cartilage damage and promoting repair. To identify and characterize effectors or regulators of cartilage remodeling in these processes, we are using culture models of primary human and mouse chondrocytes and cell lines and mouse genetic models to manipulate gene expression programs leading to matrix remodeling and subsequent chondrocyte hypertrophic differentiation, pivotal processes which both go astray in OA disease. Matrix metalloproteinases (MMP)-13, the major type II collagen-degrading collagenase, is regulated by stress-, inflammation-, and differentiation-induced signals that not only contribute to irreversible joint damage (progression) in OA, but importantly, also to the initiation/onset phase, wherein chondrocytes in articular cartilage leave their natural growth- and differentiation-arrested state. Our work points to common mediators of these processes in human OA cartilage and in early through late stages of OA in surgical and genetic mouse models.

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Registry

Crossref · 10.22203/ecm.v021a16

Cites

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Citations

Cites

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Metadata

Authors
535 East 70th Street, C. R. B., Goldring, M., Otero, M., Plumb, D., Dragomir, C., Favero, M., EI Hachem, K., Hashimoto, K., Roach, H., Olivotto, E., Borzì, R., & Marcu, K.
Venue
European Cells and Materials
Publisher
Forum Multimedia Publishing LLC
Published
2011-02-24
Volume
21
Pages
202-220
ISSN
1473-2262 (ISSN-L)
DOI
10.22203/ecm.v021a16
OpenAlex
W2155671648
Cited by
489
References
194
FWCI
15.82
Type
journal article
Language
en
Open access
gold

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