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Rod-derived cone viability signaling for the therapy of inherited retinal degenerations

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Team leader : Thierry Léveillard

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Introduction

Our efforts are focused on exploring the molecular mechanisms of the interaction between rod and cone photoreceptors and developing novel therapeutic strategies for inherited binding diseases

Presentation

After having participated to the work describing trophic interaction between rods and cones (Mohand-Saïd et al, 1998), we have identified the trophic factor rod-derived cone viability factor (RdCVF) by high content screening (Léveillard et al., 2004). The gene Nxnl1 encodes for two products by alternative splicing, RdCVF and the thioredoxin RdCVFL.


A proteomic approach revealed that the thioredoxin RdCVFL prevents the oxidation of TAU (Fridlich et al., 2009; Cronin et al. 2010) and protected rods against photo-oxidative damage (Elachouri et al., 2015). RdCVF redox signaling extends outside the eye through its paralogue Nxnl2 (Léveillard & Sahel, 2010; Jaillard et al., 2012).


Degeneration of rods in retinitis pigmentosa, the most prevalent form of genetically inherited retinal diseases leads to the loss of RdCVF expression (Reichman et al., 2010; Delyfer et al., 2011) and the secondary degeneration of cones. The loss of function of cones and presumably the central vision in human can be prevented by the administration of RdCVF (Yang et al., 2009; Byrne et al., 2014).


The mode of action of RdCVF on cones relies on the stimulation of glucose metabolism (Aït-Ali, Fridlich, Millet-Puel, Clérin et al., in press).

 


Research areas

  • Functional genomics of the retina and therapy of inherited retinal diseases




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We are looking for postdoc in molecular neuroscience and PhD student in bioinformatics

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