June 1995
Volume 36, Issue 7
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Articles  |   June 1995
Transforming growth factor-beta induces plasminogen activator inhibitor type-1 in cultured human orbital fibroblasts.
Author Affiliations
  • H J Cao
    Department of Biochemistry and Molecular Biology, Albany Medical College, NY 12208, USA.
  • M G Hogg
    Department of Biochemistry and Molecular Biology, Albany Medical College, NY 12208, USA.
  • L J Martino
    Department of Biochemistry and Molecular Biology, Albany Medical College, NY 12208, USA.
  • T J Smith
    Department of Biochemistry and Molecular Biology, Albany Medical College, NY 12208, USA.
Investigative Ophthalmology & Visual Science June 1995, Vol.36, 1411-1419. doi:
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    • Get Citation

      H J Cao, M G Hogg, L J Martino, T J Smith; Transforming growth factor-beta induces plasminogen activator inhibitor type-1 in cultured human orbital fibroblasts.. Invest. Ophthalmol. Vis. Sci. 1995;36(7):1411-1419.

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

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Abstract

PURPOSE: The level of constitutive plasminogen activator inhibitor type-1 (PAI-1) expression in cultured human orbital fibroblasts is considerably lower than that found in dermal fibroblasts. This divergence in PAI-1 expression implies differences in the pericellular proteolytic environment and, therefore, in the turnover of extracellular matrix. In this article, the authors examine the effect of transforming growth factor-beta (TGF-beta) on PAI-1 expression in orbital fibroblasts. METHODS: Human orbital and dermal fibroblasts were grown in culture. Confluent monolayers were treated with TGF-beta. PAI-1 in the extracellular matrix was quantitated by radiolabeling the cultures and electrophoresing the cellular material on SDS-PAGE. Medium content was determined by immunoprecipitation of [35S]PAI-1 with a rabbit, anti-human, polyclonal antibody. PAI-1 mRNA was determined by Northern hybridization. RESULTS: TGF-beta increased PAI-1 levels in orbital fibroblasts in a dose-dependent manner, up to 35-fold. The induction was maximal after 16 hours of treatment. The increases in extracellular matrix PAI-1 paralleled those observed in the medium. The steady state levels of the mRNA encoding the protein were upregulated by TGF-beta up to 60-fold 8 hours after the addition of TGF-beta. The fractional increase in PAI-1 expression in orbital fibroblasts was consistently greater than that observed in dermal strains. CONCLUSIONS: Exposure to TGF-beta consistently induces PAI-1 expression in orbital fibroblasts, cells that do not express the polypeptide constitutively at high levels. The effects are mediated at the pretranslational level and involve the upregulation of PAI-1 mRNA. These results suggest that TGF-beta may exert a profound regulatory influence on the pericellular proteolytic environment in orbital connective tissue.

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