Expression of cellular fibronectin and tenascin in the rabbit cornea after excimer laser photorefractive keratectomy: a 12 month study.

Abstract

An indirect immunohistochemical technique was used to monitor the expression of cellular fibronectin (cFN) and tenascin (TN) in the rabbit cornea after photorefractive keratectomy (PRK) in a 1 year follow up study. Rabbits received a 5 0 D myopic PRK, and were killed 3 days, 1, 3, 6, or 12 months after the operation. In most corneas, secondary epithelial defects appeared after the primary healing (mean 6-3 (SD 1.2) days). Corneal haze appeared a few weeks after PRK and was observed throughout the follow up. Three days after wounding an immunoreaction for cFN was observed as a bright narrow subepithelial line, but no immunoreaction for TN could be seen in the anterior third of the corneal stroma. However, at 1-6 months a similar location of immunoreactions for both cFN and TN was observed. Both were found in the anterior stroma at depths of 30-50 ,um. At 12 months, only a trace of cFN immunoreaction but no TN immunoreaction could be discerned. Our results suggest that subepithelial scar tissue contains both cFN and TN up to 12 months. (Br_J Ophthalmol 1995; 79: 65-69)

Upregulation of α9Integrin and Tenascin During Epithelial Regeneration After Debridement in the Cornea

“…Expression is first observed in the posterior stroma and then spreads to involve the entire stroma. These data are consistent with those from similar studies conducted in the corneas of rabbits (Latvala et al 1995). The work of Chiquet-Ehrismann et al (1994), studying tenascin promoter function in fibroblasts in culture that were subjected to stress or tension, suggests a possible mechanism for the increase in tenascin expression observed in response to injury i.e., the swelling of the corneal stroma that occurs after the loss of the epithelial barrier could induce tenascin expression by placing the fibroblasts under increased tension, which would then activate the tenascin promoter.…”

“…In addition, a variety of Type IV collagen genes and proteins are found in the corneal stroma and basement membrane (Ljubimov et al 1995). Fibronectin and tenascin are present, but their expression is restricted and transient (Latvala et al 1995). The complexity of the matrix is mirrored in the additional complexity of the integrins in terms of their ligand binding properties.…”

“…In situ hybridization studies of the epidermis of newts (Onda et al 1991) and of skin wound healing in rats (Aukhil et al 1996) indicate that the epithelial cells themselves produce the tenascin that is found associated with the basement membrane. Tenascin is not present in the epithelial basement membrane of the normal unwounded cornea (Latvala et al 1995;van Setten et al 1992;Tervo et al 1991). In situ hybridization analyses using tenascin RNA probes are under way to resolve whether the accumulation of tenascin beneath epithelial cells we observe in Figure 5 during restratification is due to production of the molecule by epithelial cells or by stromal fibroblasts.…”

The Influence of Corneal Stromal Matrix Proteins on the Migration of Human Corneal Fibroblasts

“…Within 12±24 hr, and before the entry of migrating corneal ®broblasts, there is an accumulation of ®bro-nectin in the stroma at the site of injury (Malley et al, 1990;van Setten et al, 1992). During the next 24±48 hr there is the additional accumulation of tenascin (van Setten et al, 1992;Latvala et al, 1995). Both of these matrix proteins are absent from the intact corneal stroma, but after PRK they remain detectable for up to a year following injury (Latvala et al, 1995).…”

Pirenoxine prevents oxidative effects of argon fluoride excimer laser irradiation in rabbit corneas: biochemical, histological and cytofluorimetric evaluations

“…The nature of this surgical follow-up is related to the complex dynamics of the wound healing response. It involves various events such as the debris removal from the margins of the wound surface, the repair of damaged structures, the production of extracellular matrix components [7,8], as well as the replacement of cellular systems, namely the repopulation of stromal keratocytes to fill apoptotic areas [9][10][11][12], and the proliferation of epithelium to cover the ablated surface [13,14].…”