• cornea;
  • fibronectin;
  • tenascin;
  • integrin;
  • CSAT;
  • anti-sense retroviral construct

During corneal development, neural crest derivatives from the periocular mesenchyme migrate into the cornea and differentiate into corneal fibroblasts. During this time, these cells interact with a variety of extracellular matrices for proper orientation and development. In the present studies, we have examined the interaction of β1 integrins on periocular mesenchyme cells (POM) and corneal fibroblasts (CF) with fibronectin and tenascin by perturbing the function of this integrin. POM and CF attached and spread to a much greater extent on fibronectin than on tenascin. An antibody against β1 integrin, CSAT, decreased spreading and attachment, and resulted in a lack of immuno-detectable β1 integrin in focal adhesions on fibronectin; few β1 positive focal adhesions were observed in cells grown on tenascin. An anti-sense retroviral construct decreased endogenous levels of β1 integrin protein, and caused decreased attachment and spreading as well as sparse, disorganized focal adhesions. These data indicate that in vitro, both POM and CF have β1 integrins that interact with fibronectin and allow them to attach and spread, while tenascin is anti-adhesive. Further studies using both of these experimental paradigms will clarify whether these interactions also occur in vivo.