April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
The dysregulation of Retinal Binding Protein 3 in the Conditional Müller Cell Ablation mouse model
Author Affiliations & Notes
  • Ling Zhu
    Save Sight Institute, Sydney University, Sydney, NSW, Australia
  • Weiyong Shen
    Save Sight Institute, Sydney University, Sydney, NSW, Australia
  • Brian Lyons
    Save Sight Institute, Sydney University, Sydney, NSW, Australia
  • Fanfan Zhou
    Faculty of Pharmacy, the University of Sydney, Sydney, NSW, Australia
  • Mark C Gillies
    Save Sight Institute, Sydney University, Sydney, NSW, Australia
  • Footnotes
    Commercial Relationships Ling Zhu, None; Weiyong Shen, None; Brian Lyons, None; Fanfan Zhou, None; Mark Gillies, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1357. doi:
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      Ling Zhu, Weiyong Shen, Brian Lyons, Fanfan Zhou, Mark C Gillies; The dysregulation of Retinal Binding Protein 3 in the Conditional Müller Cell Ablation mouse model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1357.

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

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Abstract

Purpose: The dysregulation of Retinal Binding Protein 3 (RBP3), the essential protein responsible for the intercellular exchange of retinoids, has been found to be closely related to various retinal diseases. We have investigated the changes of RBP3 expression in a novel transgenic model in which patches of Müller cell ablation can be induced. The aim of this study was to reveal the cellular communication between Müller cells and photoreceptors under stress condition and also to evaluate the A2E accumulation in the retina with RBP3 deficiency.

Methods: At different time points after the patchy ablation of Müller cells has been induced in the transgenic mice, retinal mRNA and protein samples were extracted to evaluate the expression of RBP3 at gene and protein level using realtime-PCR and immunobloting analysis. Immunohistochemistry analysis was also conducted to confirm the RBP3 changes. Retinal A2E was extracted and quantified by HPLC to be compared with that of wild type mice. Photoreceptor cells were cultured in vitro with Müller cell conditioned medium for 24 hours so as to explore the relationship between Müller cell malfunction and RBP3 deficiency in photoreceptors.

Results: We observed that the expression of RBP3 was significantly decreased at both the transcriptional and translational level after the patchy ablation of Müller cells was induced. A2E level was significantly elevated when RBP3 was dysregulated in transgenic mice compared with that of wild type mice. In vitro experiments indicated that RBP3 expression was down regulated in the presence of stressed Müller cell conditioned medium.

Conclusions: We demonstrated the in vivo and in vitro systems in which dysregulation of RBP3 in photoreceptors is driven by Müller cell malfunction and appears to be mediated by a diffusible factor(s). The deficiency of RBP3 may contribute to the A2E accumulation in the retina. Further studies on the secreting signal factor(s) of Müller cells acting on photoreceptors in retinal diseases and the potential pathogenic consequences of RBP3 dysregulation are warranted.

Keywords: 447 cell-cell communication • 603 Muller cells • 688 retina  
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