September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
The role of pigment epithelium-derived factor in the progression of primary open angle glaucoma
Author Affiliations & Notes
  • Richard J Blanch
    Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom
    NIHR Surgical Reconstruction and Microbiology Centre, University Hospitals Birmingham, Birmingham, United Kingdom
  • Lisa J Hill
    Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom
  • Jenna O'Neill
    Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom
    NIHR Surgical Reconstruction and Microbiology Centre, University Hospitals Birmingham, Birmingham, United Kingdom
  • Philip Ian Murray
    Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom
  • Imran Masood
    Birmingham MIdland Eye Centre, Birmingham, United Kingdom
  • Ann Logan
    Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom
    NIHR Surgical Reconstruction and Microbiology Centre, University Hospitals Birmingham, Birmingham, United Kingdom
  • Zubair Ahmed
    Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom
  • Footnotes
    Commercial Relationships   Richard Blanch, None; Lisa Hill, None; Jenna O'Neill, None; Philip Murray, None; Imran Masood, None; Ann Logan, None; Zubair Ahmed, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Richard J Blanch, Lisa J Hill, Jenna O'Neill, Philip Ian Murray, Imran Masood, Ann Logan, Zubair Ahmed; The role of pigment epithelium-derived factor in the progression of primary open angle glaucoma. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © 2017 Association for Research in Vision and Ophthalmology.

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Abstract

Purpose : Primary open angle glaucoma (POAG) is a chronic neurodegenerative condition characterised by RGC death, reflected in progressive loss of visual field. Pigment epithelium-derived factor (PEDF) is constitutively expressed by RGC, Muller cells and ciliary body and is both neuroprotective and axogenic for axotomised RGC.
We hypothesised that aqueous and vitreous from patients with POAG would have lower levels of PEDF than control patients and that higher aqueous levels of PEDF would be RGC-neuroprotective and therefore be associated with lower rates of glaucoma progression.

Methods : We collected aqueous from patients undergoing cataract surgery, including 39 patients with glaucoma of any cause and 38 age-matched control patients with only cataract. Clinical data on disease severity and progression was compared to enzyme-linked immunosorbent assay measurements of aqueous PEDF levels. We also collected vitreous from patients undergoing primary vitrectomy and compared patients with glaucoma (n=9) to those without (n=35).

Results : Patients with glaucoma had significantly lower vitreous PEDF levels than patients without glaucoma (5016+/-1669ng/ml vs 10883+/-452ng/ml; p<0.001). However, there were no significant differences in aqueous PEDF levels between control patients, those with glaucoma of any cause and those with POAG (1854+/-285ng/ml; 2088+/-194ng/ml; 2054+/-307ng/ml respectively). Amongst the 16 patients with POAG there was a borderline significant positive correlation between aqueous PEDF levels and the rate of visual field loss, expressed as mean deviation/year (Pearson's R2=0.2558, p=0.054).

Conclusions : Low vitreous, but not aqueous, PEDF levels are associated with the development of glaucoma from any cause. Amongst patients with POAG, higher rates of visual field progression – and therefore RGC loss – may be associated with higher PEDF levels. If confirmed, these two results may suggest different roles for PEDF in the anterior and posterior segments or - given the known neuroprotective properties of PEDF - low levels may predispose patients to neurodegeneration, but RGC compromise may increase PEDF levels as a compensatory mechanism attempting to prevent cell death.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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