July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Aniridia and PAX6: The foundations for an RNA therapy
Author Affiliations & Notes
  • Athanasios Papadimitropoulos
    Eye and Vision Science, University of Liverpool, IACD, Liverpool, United Kingdom
  • Lauriane N Roux
    Hôpital Saint-Louis, Paris, France
  • David C Blakey
    MiNA Therapeutics, London, United Kingdom
  • Daniel Aberdam
    Hôpital Saint-Louis, Paris, France
  • Colin Willoughby
    Eye and Vision Science, University of Liverpool, IACD, Liverpool, United Kingdom
    Genomic Medicine Group, Ulster University, Biomedical Sciences Research Institute, Ulster, United Kingdom
  • Kevin Hamill
    Eye and Vision Science, University of Liverpool, IACD, Liverpool, United Kingdom
  • Footnotes
    Commercial Relationships   Athanasios Papadimitropoulos, None; Lauriane Roux, None; David Blakey, MiNA Therapeutics (E); Daniel Aberdam, None; Colin Willoughby, None; Kevin Hamill, None
  • Footnotes
    Support  Fight for Sight [UK]
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 3400. doi:
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      Athanasios Papadimitropoulos, Lauriane N Roux, David C Blakey, Daniel Aberdam, Colin Willoughby, Kevin Hamill; Aniridia and PAX6: The foundations for an RNA therapy. Invest. Ophthalmol. Vis. Sci. 2019;60(9):3400.

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

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Abstract

Purpose : Aniridia is a congenital panocular disease caused by mutations leading to haploinsufficiency of the transcription factor Paired Box Protein 6 (PAX6). Small-activating RNAs (saRNA) have been used to increase expression of genes in a variety of different contexts. Here we hypothesised that saRNAs could be used to increase the levels of the wild-type PAX6 transcript and rescue the phenotype of PAX6+/- cells.

Methods : A panel of bioinformatically designed saRNAs were designed to target different regions of the PAX6 promoter. These were then tested in three human cell lines of clinical relevance: human Telomerase-immortalised Corneal Epithelial cells (hTCEpi), human Telomerase-immortalised Limbal Epithelial Stem cells, (L-TSC) and an L-TSC PAX6+/- cell line with a CRISPR/Cas9 introduced premature termination codon mutation. After saRNA treatment the RNA and protein levels of PAX6 were quantified by 2-step RT-qPCR and Western Blot respectively. For the top saRNA candidates the expression levels of genes that are downstream targets of PAX6 were quantified and the ability of saRNAs to rescue cell behaviour phenotypes of cell detachment and migration on the PAX6+/- cells were assessed.

Results : In hTCEpi, most of saRNA showed a trend towards upregulation of PAX6 transcript levels, with three reaching a statistically significant 2-fold or greater increase (n=3, p<0.05). One of these candidate saRNAs displayed significant upregulation (2.0±0.5 fold change, n=3, p<0.05) across all three (hTCEpi, L-TSC and L-TSC PAX6+/-) lines . Steady-state whole cell extract PAX6 protein levels did not precisely match the transcript abundance data. However, in the PAX6+/- L-TSC line that was developed to resemble the haploinsufficiency phenotype, the gene expression of four downstream targets of PAX6 was rescued, and phenotypic correction of aberrant cell adhesion and motility behaviour was achieved through saRNA treatment.

Conclusions : Our results support the hypothesis that increasing PAX6 transcript levels with saRNAs can rescue aspects of phenotype of PAX6+/- cells. We were able to identify at least one saRNA that shows promise for future investigation towards a possible saRNA therapy for aniridia.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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