Metalloproteinases and their inhibitors in angiogenesis

2003 ◽  
Vol 5 (23) ◽  
pp. 1-39 ◽  
Author(s):  
Marc A. Lafleur ◽  
Madeleine M. Handsley ◽  
Dylan R. Edwards
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Cell Function ◽  
Proteolytic Enzymes ◽  
Biologically Relevant ◽  
Physiological Processes ◽  
Adam Family ◽  
Angiogenic Inhibitors ◽  
Membrane Type

Angiogenesis, the formation of new blood vessels from the pre-existing vasculature, is an integral part of physiological processes such as embryonic development, the female reproductive cycle and wound healing. Angiogenesis is also central to a variety of pathologies including cancer, where it is recognised as being crucial for the growth of solid tumours. Matrix metalloproteinases (MMPs) are a family of soluble and membrane-anchored proteolytic enzymes that can degrade components of the extracellular matrix (ECM) as well as a growing number of modulators of cell function. Several of the MMPs, most notably MMP-2 and -9 and membrane-type-1 MMP (MT1-MMP), have been linked to angiogenesis. Potential roles for these proteases during the angiogenic process include degradation of the basement membrane and perivascular ECM components, liberation of angiogenic factors, production of endogenous angiogenic inhibitors, and the unmasking of cryptic biologically relevant sites in ECM components. This review brings together what is currently known about the functions of the MMPs and the closely related adamalysin metalloproteinase (ADAM) family in angiogenesis, and discusses how this information might be useful in manipulation of the angiogenic process, with a view to controlling aberrant neovascularisation.

The extracellular matrix of lip wounds in fetal, neonatal and adult mice

Development ◽  
1991 ◽  
Vol 112 (2) ◽  
pp. 651-668
Author(s):  
D.J. Whitby ◽  
M.W. Ferguson
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Cell Migration ◽  
Inflammatory Response ◽  
Cell Function ◽  
Chondroitin Sulphate ◽  
Scar Formation ◽  
Collagen Types ◽  
Cellular Mechanisms ◽  
Collagen Formation

Wound healing in the fetus occurs rapidly, by a regenerative process and without an inflammatory response, resulting in complete restitution of normal tissue function. By contrast, in the adult, wounds heal with scar formation, which may impair function and inhibit further growth. The cellular mechanisms underlying these differing forms of wound healing are unknown but the extracellular matrix (ECM), through its effects on cell function, may play a key role. We have studied the ECM in upper lip wounds of adult, neonatal and fetal mice at days 14, 16 and 18 of gestation. The spatial and temporal distribution of collagen types I, III, IV, V and VI, fibronectin, tenascin, laminin, chondroitin and heparan sulphates were examined immunohistochemically. Results from the fetal groups were essentially similar whilst there were distinct differences between fetus, neonate and adult. Fibronectin was present at the surface of the wound in all groups at 1 h post-wounding. Tenascin was also present at the wound surface but the time at which it was first present differed between fetus (1 h), neonate (12 h) and adult (24 h). The time of first appearance paralleled the rate of wound healing which was most rapid in the fetus and slowest in the adult. Tenascin inhibits the cell adhesion effect of fibronectin and during development the appearance of tenascin correlates with the initiation of cell migration. During wound healing the appearance of tenascin preceded cell migration and the rapid closure of fetal wounds may be due to the early appearance of tenascin in the wound. Collagen types I, III, IV, V and VI were present in all three wound groups but the timing and pattern of collagen deposition differed, with restoration of the normal collagen pattern in the fetus and a scar pattern in the adult. This confirms that lack of scarring in fetal wounds is due to the organisation of collagen within the wound and not simply lack of collagen formation. The distribution of chondroitin sulphate differed between normal fetal and adult tissues and between fetal and adult wounds. Its presence in the fetal wound may alter collagen fibril formation. No inflammatory response was seen in the fetal wounds. The differences in the ECM of fetal and adult wounds suggests that it may be possible to alter the adult wound so that it heals by a fetal-like process without scar formation, loss of tissue function or restriction of growth.

scholarly journals Membrane Type 1 Matrix Metalloproteinase Digests Interstitial Collagens and Other Extracellular Matrix Macromolecules

1997 ◽  
Vol 272 (4) ◽  
pp. 2446-2451 ◽  
Author(s):  
Eiko Ohuchi ◽  
Kazushi Imai ◽  
Yutaka Fujii ◽  
Hiroshi Sato ◽  
Motoharu Seiki ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Interstitial Collagens ◽  
Membrane Type

scholarly journals Egr-1 Mediates Extracellular Matrix-driven Transcription of Membrane Type 1 Matrix Metalloproteinase in Endothelium

1999 ◽  
Vol 274 (32) ◽  
pp. 22679-22685 ◽  
Author(s):  
Tara L. Haas ◽  
David Stitelman ◽  
Sandra J. Davis ◽  
Suneel S. Apte ◽  
Joseph A. Madri
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Membrane Type

scholarly journals Proactive for invasion: Reuse of matrix metalloproteinase for structural memory

2016 ◽  
Vol 213 (1) ◽  
pp. 11-13 ◽  
Author(s):  
Erika Gucciardo ◽  
Mohammad Mobashir ◽  
Kaisa Lehti
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Spatial Memory ◽  
Cytoplasmic Domain ◽  
Cell Biol ◽  
Membrane Type ◽  
Migratory Cells ◽  
Structural Memory

Migratory cells translocate membrane type-1 matrix metalloproteinase (MT1-MMP) to podosomes or invadosomes to break extracellular matrix barriers. In this issue, El Azzouzi et al. (2016. J. Cell. Biol. http://dx.doi.org/10.1083/jcb.201510043) describe an unexpected function for the MT1-MMP cytoplasmic domain in imprinting spatial memory for podosome reformation via assembly in membrane islets.

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