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Re-formation of the Epidermal—Dermal Junction during Wound Healing

  • Chapter
The Molecular and Cellular Biology of Wound Repair

Abstract

The relationship between keratinocytes and the extracellular matrix upon which they rest is complex and only beginning to be understood. Keratinocytes are capable of synthesizing many of the extracellular matrix molecules that are most closely related to their cell surface, such as the bullous pemphigoid antigen (Woodley and Régnier, 1979; Stanley et al., 1980; Woodley et al., 1980a, 1982) laminin (Stanley et al., 1982c), the epidermolysis bullosa acquisita antigen (Woodley et al., 1985b), and fibronectin (O’Keefe et al., 1984; Kubo et al.., 1984). Thus, it is clear that keratinocytes directly influence their extracellular matrix composition. Furthermore, it is becoming apparent that cellular behavior can be modified by contact with a given extracellular matrix molecule. For example, mammary epithelial cells have a decreased requirement for epidermal growth factor when cultured on type IV (basement membrane) collagen as compared with type I (interstitial) collagen (Salomon et al., 1981). The influence on cellular behavior by contact with matrix molecules is often referred to as cell-matrix interactions. The cell-matrix interactions that apply to the ker-atinocyte may be viewed as a self-contained system, since the keratinocytes synthesize and extracellularly deposit their own matrix components, which in turn directly affects the behavior of cells in contact with the cell plasma membrane.

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  1. Department of Dermatology, University of North Carolina, Chapel Hill, North Carolina, 27514, USA

    David T. Woodley & Robert A. Briggaman

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  1. David T. Woodley
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  1. National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado, USA

    R. A. F. Clark  & P. M. Henson  & 

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Woodley, D.T., Briggaman, R.A. (1988). Re-formation of the Epidermal—Dermal Junction during Wound Healing. In: Clark, R.A.F., Henson, P.M. (eds) The Molecular and Cellular Biology of Wound Repair. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1795-5_23

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  • DOI: https://doi.org/10.1007/978-1-4615-1795-5_23

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