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Open AccessJournal ArticleDOI

Matrix Metalloproteinases: A Review

TLDR
The present review discusses in detail the primary structures and the overlapping yet distinct substrate specificities of MMPs as well as the mode of activation of the unique MMP precursors.
Abstract
Matrix metalloproteinases (MMPs) are a family of nine or more highly homologous Zn(++)-endopeptidases that collectively cleave most if not all of the constituents of the extracellular matrix. The present review discusses in detail the primary structures and the overlapping yet distinct substrate specificities of MMPs as well as the mode of activation of the unique MMP precursors. The regulation of MMP activity at the transcriptional level and at the extracellular level (precursor activation, inhibition of activated, mature enzymes) is also discussed. A final segment of the review details the current knowledge of the involvement of MMP in specific developmental or pathological conditions, including human periodontal diseases.

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Citations
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Journal ArticleDOI

Matrix metalloproteinases and their inhibitors in connective tissue remodeling.

TL;DR: Latency is overcome by physical, chemical, and enzymatic treatments that separate the cysteine residue from the zinc Expression of the metalloproteinases is switched on by a variety of agents acting through regulatory elements of the gene, particularly the AP‐1 binding site.
Journal ArticleDOI

Matrix metalloproteinases and the regulation of tissue remodelling

TL;DR: Recent studies in mice and flies point to essential roles of MMPs as mediators of change and physical adaptation in tissues, whether developmentally regulated, environmentally induced or disease associated.
Journal ArticleDOI

A matrix metalloproteinase expressed on the surface of invasive tumour cells

TL;DR: The cloning of the complemen-tary DNA encoding a new matrix metalloproteinase with a potential transmembrane domain is reported, which may trigger invasion by tumour cells by activating pro-gelatinase A on the tumour cell surface.
Journal ArticleDOI

MMP-9/Gelatinase B Is a Key Regulator of Growth Plate Angiogenesis and Apoptosis of Hypertrophic Chondrocytes

TL;DR: Transplantation of wild-type bone marrow cells rescues vascularization and ossification in gelatinase B-null growth plates, indicating that these processes are mediated by gelatinaseB-expressing cells of bone marrow origin, designated chondroclasts.
Journal ArticleDOI

Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy.

TL;DR: The hypothesis that idiopathic pulmonary fibrosis is a fibrotic rather than an inflammatory disease is examined, and the therapeutic implications of these findings are discussed.
References
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Journal ArticleDOI

Tissue Destruction by Neutrophils

TL;DR: With increasing frequency, the human neutrophil is being implicated as a mediator of tissue-destructive events in inflammatory diseases ranging from rheumatoid arthritis and myocardial reperfusion injury to respiratory distress syndromes, blistering skin disorders, and ulcerative colitis.
Journal ArticleDOI

Matrix metalloproteinases and their inhibitors in connective tissue remodeling.

TL;DR: Latency is overcome by physical, chemical, and enzymatic treatments that separate the cysteine residue from the zinc Expression of the metalloproteinases is switched on by a variety of agents acting through regulatory elements of the gene, particularly the AP‐1 binding site.
Journal ArticleDOI

Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor.

TL;DR: Results strongly suggest that AP-1 is at the receiving end of a complex pathway responsible for transmitting the effects of phorbol ester tumor promoters from the plasma membrane to the transcriptional machinery.
Book ChapterDOI

Plasminogen activators, tissue degradation, and cancer.

TL;DR: This chapter describes two types of plasminogen activators—namely, the urokinase-type plasMinogen activator (u-PA) and the tissue- type plasmineg activator(t-PA), which are essentially different gene products.
Journal ArticleDOI

Metastatic potential correlates with enzymatic degradation of basement membrane collagen.

TL;DR: The cell lines with the highest incidence of spontaneous metastasis exhibit the greatest level of type IV collagen-degrading activity in two different assays using either living cells or media obtained from cell cultures.
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