August 1993
Volume 34, Issue 9
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Articles  |   August 1993
Inhibition of retinal pigment epithelial cell migration and proliferation with monoclonal antibodies against the beta 1 integrin subunit during wound healing in organ culture.
Author Affiliations
  • G J Hergott
    Department of Anatomy, University of Toronto, Ontario, Canada.
  • H Nagai
    Department of Anatomy, University of Toronto, Ontario, Canada.
  • V I Kalnins
    Department of Anatomy, University of Toronto, Ontario, Canada.
Investigative Ophthalmology & Visual Science August 1993, Vol.34, 2761-2768. doi:
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      G J Hergott, H Nagai, V I Kalnins; Inhibition of retinal pigment epithelial cell migration and proliferation with monoclonal antibodies against the beta 1 integrin subunit during wound healing in organ culture.. Invest. Ophthalmol. Vis. Sci. 1993;34(9):2761-2768.

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Abstract

PURPOSE: To investigate the effect that antibodies against the beta 1 subunit of integrin, a cell-surface extracellular matrix receptor, would exert on chick embryo retinal pigment epithelial (RPE) cells maintained in organ culture after mechanical wounding of the epithelium. METHODS: RPE cells maintained in organ culture in the presence of antibodies against the beta 1 subunit of integrin were observed to quantify their spreading and migration. Antibodies against proliferating cell nuclear antigen (PCNA) were used to assess cell proliferation under the experimental conditions. RESULTS: In the presence of monoclonal antibodies against the beta 1 subunit of integrin, cell migration is inhibited whereas the initial cell spreading response still occurs. This implies that the RPE cells along the wound edge use different mechanisms in interacting with the substratum in spreading and in migration. Moreover, the RPE cells along the wound edge of cultures in which migration is inhibited do not express PCNA. Higher concentrations of the anti-integrin antibodies, however, are required to inhibit cell proliferation than to inhibit cell migration. CONCLUSIONS: These results suggest that specific cell-substratum interactions may be involved in the initiation of a proliferative response to wound healing in this model system.

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