February 1992
Volume 33, Issue 2
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Articles  |   February 1992
Adhesion complex formation after small keratectomy wounds in the cornea.
Author Affiliations
  • E L Stock
    Cornea and External Eye Disease Laboratory, VA Lakeside Medical Center, Chicago, Illinois.
  • M A Kurpakus
    Cornea and External Eye Disease Laboratory, VA Lakeside Medical Center, Chicago, Illinois.
  • B Sambol
    Cornea and External Eye Disease Laboratory, VA Lakeside Medical Center, Chicago, Illinois.
  • J C Jones
    Cornea and External Eye Disease Laboratory, VA Lakeside Medical Center, Chicago, Illinois.
Investigative Ophthalmology & Visual Science February 1992, Vol.33, 304-313. doi:
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    • Get Citation

      E L Stock, M A Kurpakus, B Sambol, J C Jones; Adhesion complex formation after small keratectomy wounds in the cornea.. Invest. Ophthalmol. Vis. Sci. 1992;33(2):304-313.

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Abstract

The adhesion complex of the corneal epithelium consists of the hemidesmosome and its associated structures, such as anchoring filaments, lamina densa of the basement membrane, and anchoring fibrils. It contributes to the adhesion of the corneal epithelium to Bowman's layer. To understand the adhesion complex better, an electron microscopic and immunofluorescence analysis was done of the reformation of the adhesion complex in small (1 mm) keratectomy wounds in the guinea pig cornea. In these wounds, the epithelium, hemidesmosomes, basal lamina, anchoring fibrils, and anterior stroma were removed. The wound bed was epithelialized completely by 24 hr after wounding. Immunofluorescence analyses involved the use of antibodies against plaque components of the hemidesmosome, an antibody against laminin, and an antibody against the collagen VII component of anchoring fibrils. At 18 hr after wounding, there was no morphologic evidence of hemidesmosomes at the epithelial-stromal interface. At 24 hr, hemidesmosomes were observed, with or without subjacent lamina densa. Furthermore, plaque components were detected by immunofluorescence in those cells in contact with the wound bed. In contrast, no type VII collagen was detected. On day 7, collagen VII, laminin, and bullous pemphigoid autoantibody markers colocalized along the wound bed as determined by immunofluorescence. However, at the ultrastructural level, even though the lamina densa of the basal lamina was observed primarily where hemidesmosomes were present, it remained incomplete. In this study, the precise temporal sequence in which components are incorporated into the assembling adhesion complex was described during wound healing. Furthermore, the possibility that the hemidesmosomal plaque nucleates the formation of the underlying basal lamina was discussed.

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