March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Anti-Connective Tissue Growth Factor Antibody Therapy Combats Expression of Fibrotic Genes in Glaucoma
Author Affiliations & Notes
  • Deborah M. Wallace
    School Medicine & Medical Science,
    University College Dublin, Dublin, Ireland
    Dept. Of Ophthalmology, Mater Misericordiae University Hospital, Dublin, Ireland
  • Abbot F. Clark
    Cell Biology & Anatomy, University of North Texas HSC, Fort Worth, Texas
  • Noelynn Oliver
    FibroGen Inc, San Francisco, California
  • John K. Crean
    School of Biomolecular & Biomedical Science, Conway Inst.,
    University College Dublin, Dublin, Ireland
  • Colm J. O'Brien
    Ophthalmology, Mater Misericordiae Univ Hospital, Dublin, Ireland
    School of Medicine and Medical Science, University College Dublin, Ireland
  • Footnotes
    Commercial Relationships  Deborah M. Wallace, None; Abbot F. Clark, None; Noelynn Oliver, FibroGen Inc. (E); John K. Crean, None; Colm J. O'Brien, None
  • Footnotes
    Support  Health Research Board Ireland (HRA_POR/2010/129) & International Glaucoma Association
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6945. doi:
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    • Get Citation

      Deborah M. Wallace, Abbot F. Clark, Noelynn Oliver, John K. Crean, Colm J. O'Brien; Anti-Connective Tissue Growth Factor Antibody Therapy Combats Expression of Fibrotic Genes in Glaucoma. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6945.

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

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Abstract

Purpose: : We have previously demonstrated elevated levels of connective tissue growth factor (CTGF) in the aqueous humour of Pseudoexfoliation glaucoma (PXFG) and Primary open angle glaucoma (POAG) patients compared to controls. CTGF was also shown to upregulate fibrillin-1 (a component of PXF-material) expression in cultured human trabecular meshwork (TM) cells. The purpose of this study was to investigate the therapeutic potential of anti-CTGF immunotherapy in PXFG and POAG in combating fibrosis using oxidative stress and aqueous humour samples as stimuli in primary TM and primary lamina cribrosa (LC) cells.

Methods: : Aqueous humour samples from PXFG, POAG and control patients (n=3) were applied to porcine TM and human LC cells in the presence or absence of the monoclonal anti-CTGF antibody FG-3019 (10μM) (FibroGen Inc, South San Francisco, CA). Hydrogen peroxide (200μM H2O2, a subtoxic dose as determined by crystal violet assay) was used as a glaucoma-like (oxidative stress) stimulus +/- FG-3019. CTGF, fibrillin-1 and fibronectin-1 expression levels were assessed by quantitative PCR using gene specific exon-exon spanning primers. IgG antibody (10μM) was included as a negative control in both sets of experiments.

Results: : Results showed that incubation of LC and TM cells with aqueous humour from both PXFG and POAG patients induced a significant (P<0.05) increase in expression of CTGF, fibrillin 1 and fibronectin 1. This fibrotic response was significantly reduced by the inclusion of FG-3019 (P<0.05). Similar results were obtained for oxidative stress treatment of LC and TM cells (P<0.05).

Conclusions: : The anti-CTGF antibody FG-3019 is effective in blocking CTGF, fibrillin 1 and fibronectin 1 production. These observed anti-fibrotic effects support a pathologically significant role for the use of anti-CTGF immunotherapy as a possible approach for treatment of PXFG and POAG.

Keywords: extracellular matrix • trabecular meshwork • lamina cribrosa 
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