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Repair of the corneal epithelial adhesion structures following keratectomy wounds in diabetic rabbits
Author(s) -
Azar Dimitri T.,
Gipson Ilene K.
Publication year - 1989
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.1989.tb07097.x
Subject(s) - hemidesmosome , basement membrane , basal lamina , anchoring fibrils , lamina lucida , laminin , wound healing , pathology , lamina densa , type iv collagen , epithelium , chemistry , corneal epithelium , medicine , anatomy , ultrastructure , biology , microbiology and biotechnology , surgery , extracellular matrix
In corneal tissue from a diabetic patient 15 months after delayed epithelial healing following vitrectomy surgery, electron microscopy revealed a discontinuous basement membrane; immunohistochemically, fibronectin was present in the basement membrane zone. To determine whether alterations in repair of the basement membrane, anchoring fibrils and hemidesmo‐somes occur in wounds in diabetics, we studied the pattern of histochemical localization of bullous pemphigoid antigen (the intracellular hemidesmosome plaque component), laminin and type VII collagen (the anchoring fibril collagen) in alloxan‐induced diabetic rabbits following superficial keratectomy. Ultrastructural studies of basal laminae and hemidesmosomes also were performed. Epithelial wound closure was complete by 66–72 h after 7‐mm superficial keratectomies. Type VII collagen localized at the base of the epithelium at the wound periphery by 66 h, appearing as a beaded line underlying the epithelium; at 1 week, as in control rabbits, the localization zone extended across the wound bed. Polyclonal antibodies to laminin and bullous pemphigoid antigen showed similar localization. Small segments of basal laminae were noted by electron microscopy of the wound periphery as early as 66 h post‐kera‐tectomy. By 2 weeks, an increase in hemidesmosomes associated with segments of discontinuous basal lamina was apparent. No obvious differences in the time or pattern of re‐appearance of the adhesion complex in keratectomy wounds could be discerned between normoglycemic and hyperglycemic rabbits. Thus, healing defects in diabetics may be due to factors other than reassembly of adhesion structures.