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      Interactions between extracellular matrix and growth factors in wound healing.

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          Abstract

          Dynamic interactions between growth factors and extracellular matrix (ECM) are integral to wound healing. These interactions take several forms that may be categorized as direct or indirect. The ECM can directly bind to and release certain growth factors (e.g., heparan sulfate binding to fibroblast growth factor-2), which may serve to sequester and protect growth factors from degradation, and/or enhance their activity. Indirect interactions include binding of cells to ECM via integrins, which enables cells to respond to growth factors (e.g., integrin binding is necessary for vascular endothelial growth factor-induced angiogenesis) and can induce growth factor expression (adherence of monocytes to ECM stimulates synthesis of platelet-derived growth factor). Additionally, matrikines, or subcomponents of ECM molecules, can bind to cell surface receptors in the cytokine, chemokine, or growth factor families and stimulate cellular activities (e.g., tenascin-C and laminin bind to epidermal growth factor receptors, which enhances fibroblast migration). Growth factors such as transforming growth factor-beta also regulate the ECM by increasing the production of ECM components or enhancing synthesis of matrix degrading enzymes. Thus, the interactions between growth factors and ECM are bidirectional. This review explores these interactions, discusses how they are altered in difficult to heal or chronic wounds, and briefly considers treatment implications.

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          Author and article information

          Journal
          Wound Repair Regen
          Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
          Wiley
          1524-475X
          1067-1927
          March 27 2009
          : 17
          : 2
          Affiliations
          [1 ] Department of Obstetrics and Gynecology, University of Florida, Gainesville, 32610-0294, USA. schultzg@ufl.edu
          Article
          WRR466
          10.1111/j.1524-475X.2009.00466.x
          19320882
          90ef9b41-a2d9-4e85-b748-2ef9fda7ea6e
          History

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