April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
TCF Activation Correlates With Downregulation of Keratan Sulfate Biosynthesis
Author Affiliations & Notes
  • M. L. Funderburgh
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
  • M. M. Mann
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
  • J. L. Funderburgh
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
  • Footnotes
    Commercial Relationships  M.L. Funderburgh, None; M.M. Mann, None; J.L. Funderburgh, None.
  • Footnotes
    Support  NIH Grants EY09368 and 30-EY08098. Research to Prevent Blindness
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 6205. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      M. L. Funderburgh, M. M. Mann, J. L. Funderburgh; TCF Activation Correlates With Downregulation of Keratan Sulfate Biosynthesis. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6205.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : Keratan sulfate (KS) is uniquely abundant in the corneal stroma and is essential for corneal transparency. Biosynthesis of KS is a function of stromal keratocytes and is markedly downregulated during wound healing and when the cells are cultured in vitro. The expression of glycosyl- and sulfotransferase enzymes required for KS biosynthesis is rapidly regulated by exposure of keratocytes to cytokines or serum, but the signaling mechanism involved in this downregulation is not understood. In the current study we sought to determine if Wnt signaling is involved KS regulation.

Methods: : Primary bovine keratocytes were treated in serum free media with cytokines and inhibitors regulating Wnt signaling pathways. Wnt signaling was examined by TCF-driven luciferase expression and cyclin D1 activation. KS biosynthesis was monitored by KS immunoblotting and by qPCR for mRNA levels of KS biosynthetic enzymes.

Results: : Synthetic Wnt agonist FH535 downregulated KS biosynthesis and mRNA for KS biosynthetic enzymes in a dose-dependent manner. Inhibitors which block degradation of beta catenin, BIO and M132, upregulated cyclin D1 indicating activation of TCF signaling. These inhibitors also produced rapid downregulation of glycosyl transferase B3GnT7, and the sulfotransferases CHST1 and CHST6, enzymes thought to be involved in KS synthesis.

Conclusions: : Downregulation of KS and of the mRNA for KS biosynthetic enzymes correlates with activation of signaling via the canonical Wnt signaling pathway involving activation of the TCF transcription factor by nuclear translocation of beta catenin. These results lend support to the hypothesis that the Wnt signaling pathway is involved in control of KS biosynthesis.

Keywords: extracellular matrix • signal transduction • proteoglycans/glycosaminoglycans 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×