March 1999
Volume 40, Issue 3
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Articles  |   March 1999
Regulation of gelatinase B production in corneal cells is independent of autocrine IL-1alpha.
Author Affiliations
  • P Bargagna-Mohan
    New England Medical Center, Department of Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
  • K J Strissel
    New England Medical Center, Department of Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
  • M E Fini
    New England Medical Center, Department of Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Investigative Ophthalmology & Visual Science March 1999, Vol.40, 784-789. doi:
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    • Get Citation

      P Bargagna-Mohan, K J Strissel, M E Fini; Regulation of gelatinase B production in corneal cells is independent of autocrine IL-1alpha.. Invest. Ophthalmol. Vis. Sci. 1999;40(3):784-789.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: The matrix metalloproteinase gelatinase B is synthesized by cells at the leading edge of the corneal epithelium migrating to heal a wound. Recent data from the authors' laboratory suggest that excessive synthesis contributes to repair defects. The goal of the study reported here was to investigate mechanisms controlling gelatinase B production by corneal epithelial cells. METHODS: Freshly isolated cultures of corneal epithelial cells and early passage stromal fibroblasts from rabbit were used for these studies. RESULTS: In a previous study, it was found that the cytokine interleukin (IL)-1alpha is released into the culture medium of corneal epithelial cells more efficiently when they are plated at low density with limited cell-cell contact than when plated at high density. In this study, we show that production of gelatinase B by these cells is similarly affected by cell plating density. However, it is further demonstrated that these two events are not dependent on one another but occur in parallel: IL-1alpha does not regulate gelatinase B production (synthesis), nor was there evidence that any other secreted autocrine cytokine acts as mediator. Instead, our data suggest that gelatinase B production is downregulated directly by high cell density and indicate a connection to the level of protein kinase C activity. Nevertheless, the anticancer agent suramin, which blocks collagenase synthesis by interfering with autocrine cytokine-receptor interactions, still inhibits synthesis of gelatinase B. CONCLUSIONS: Unlike collagenase synthesis by corneal stromal fibroblasts, production (synthesis) of gelatinase B does not appear to be controlled by secreted autocrine cytokines but can still be inhibited by suramin. Suramin may make an effective therapeutic agent for controlling pathologic overproduction of gelatinase B in corneal ulcers.

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