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Wound healing table

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Functions of elastase, cathepsin G, plasmin and MMP- 2 in the wound repair process

 

Elastase Cathepsin G Plasmin MMP-2

• Stimulates production of fibrin clot that acts as a provisional matrix in the wound bed.

 

• Promotes infiltration of inflammatory cells e.g. neutrophils to the wound site by activating cytokines and inducing their secretion from various cell types.

 

• Debrides the wound by phagocytosis of debris, microbes and degraded matrix components.

 

• Down-regulates inflammation by inactivation of cytokines.


• Promotes endothelial cell migration through the fibrin rich clot during angiogenesis.

 

• Down-regulates angiogenesis.

 

• Degrades the provisional matrix and remodels ECM (extracellular matrix) components into a mature scar.

• Stimulates production of fibrin clot that acts as a provisional matrix in the wound bed.

 

• Promotes migration of neutrophils and monocytes into the wound bed.

• Debrides the wound by phagocytosis of debris, microbes and degraded matrix components.

• Degrades fibrin clot (fibrinolysis) allowing migration of endothelial cells (angiogenesis), fibroblasts (granulation tissue formation) and keratinocytes (re-epithelialization) into the provisional matrix.

 

• Indirectly promotes the remodelling phase of wound repair by activating pro-MMPs (metalloproteinases).

• Promotes endothelial cell migration through the fibrin rich clot during angiogenesis.

 

• Remodels the ECM into a mature scar.

 

Because all of these proteases have the ability to degrade all the components within the ECM (e.g. fibronectin, vitronectin, laminin) they can cause extensive damage to the provisional ECM when present in excess levels. As a result no scaffold is available for keratinocyte adhesion and migration, which results in retarded re-epithelialization.

 

In addition, the ECM fragments formed during matrix damage act as chemotactic factors that attract additional inflammatory cells such as neutrophils to the wound site. These cells release extra proteases, which exacerbate matrix damage and cause the wound to become stuck in a prolonged inflammatory phase.


Lastly, excess levels of these proteases can impair wound repair processes such as angiogenesis by degrading important cell signalling molecules such as growth factors e.g. VEGF.