French Academy of science

Paris, France

French Academy of science

Paris, France

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Froger N.,French Institute of Health and Medical Research | Froger N.,University Pierre and Marie Curie | Froger N.,French National Center for Scientific Research | Jammoul F.,French Institute of Health and Medical Research | And 40 more authors.
Advances in Experimental Medicine and Biology | Year: 2013

Retinal ganglion cells (RGCs) are spiking neurons, which send visual information to the brain, through the optic nerve. RGC degeneration occurs in retinal diseases, either as a primary process or secondary to photoreceptor loss. Mechanisms involved in this neuronal degeneration are still unclear and no drugs directly targeting RGC neuroprotection are yet available. Here, we show that taurine is one factor involved in preserving the RGC survival. Indeed, a taurine depletion induced by the antiepileptic drug, vigabatrin, was incriminated in its retinal toxicity leading to the RGC loss. Similarly, we showed that RGC degeneration can be induced by pharmacologically blocking the taurine-transporter with the chronic administration of a selective inhibitor, which results in a decrease in the taurine levels both in the plasma and in the retinal tissue. Finally, we found that taurine can directly prevent RGC degeneration, occurring either in serum-deprived pure RGC cultures or in animal models presenting an RGC loss (glaucomatous rats and the P23H rats, a model for retinitis pigmentosa ). These data suggest that the retinal taurine level is a crucial marker to prevent RGC damage in major retinal diseases. © Springer Science+Business Media New York 2013.


Froger N.,French Institute of Health and Medical Research | Froger N.,University Pierre and Marie Curie | Froger N.,French National Center for Scientific Research | Moutsimilli L.,French Institute of Health and Medical Research | And 37 more authors.
Progress in Retinal and Eye Research | Year: 2014

Taurine is the most abundant amino acid in the retina. In the 1970s, it was thought to be involved in retinal diseases with photoreceptor degeneration, because cats on a taurine-free diet presented photoreceptor loss. However, with the exception of its introduction into baby milk and parenteral nutrition, taurine has not yet been incorporated into any commercial treatment with the aim of slowing photoreceptor degeneration. Our recent discovery that taurine depletion is involved in the retinal toxicity of the antiepileptic drug vigabatrin has returned taurine to the limelight in the field of neuroprotection. However, although the retinal toxicity of vigabatrin principally involves a deleterious effect on photoreceptors, retinal ganglion cells (RGCs) are also affected. These findings led us to investigate the possible role of taurine depletion in retinal diseases with RGC degeneration, such as glaucoma and diabetic retinopathy. The major antioxidant properties of taurine may influence disease processes. In addition, the efficacy of taurine is dependent on its uptake into retinal cells, microvascular endothelial cells and the retinal pigment epithelium. Disturbances of retinal vascular perfusion in these retinal diseases may therefore affect the retinal uptake of taurine, resulting in local depletion. The low plasma taurine concentrations observed in diabetic patients may further enhance such local decreases in taurine concentration. We here review the evidence for a role of taurine in retinal ganglion cell survival and studies suggesting that this compound may be involved in the pathophysiology of glaucoma or diabetic retinopathy. Along with other antioxidant molecules, taurine should therefore be seriously reconsidered as a potential treatment for such retinal diseases. © 2014 Elsevier Ltd.


Rosolen S.-G.,Reseau Europeen dOphtalmologie Veterinaire et de Vision Animale | Rosolen S.-G.,Voltaire | Rosolen S.-G.,French Institute of Health and Medical Research | Rosolen S.-G.,University Pierre and Marie Curie | And 19 more authors.
Advances in Experimental Medicine and Biology | Year: 2013

In the 70s, the amino acid taurine was found essential for photoreceptor survival. Recently, we found that taurine depletion can also trigger retinal ganglion cell degeneration both in vitro and in vivo . Therefore, evaluation of taurine levels could be a crucial biomarker for different pathologies of retinal ganglion cells such as glaucoma. Because different breeds of dog can develop glaucoma, we performed taurine measurements on plasma and aqueous humour samples from pet dogs. Here, we exposed results from a pilot study on normal selected breed of pet dogs, without any ocular pathology. Samples were collected by veterinarians who belong to the Réseau Européen d'Ophtalmologie Vétérinaire et de Vision Animale . Following measurements by high-performance liquid chromatography (HPLC), the averaged taurine concentration was 162.3 μ M in the plasma and 51.8 μ M in the aqueous humour. No correlation was observed between these two taurine concentrations, which exhibited a ratio close to 3. Further studies will determine if these taurine concentrations are changed in glaucomatous dogs. © Springer Science+Business Media New York 2013.


Sahel J.A.,French Institute of Health and Medical Research | Sahel J.A.,University Pierre and Marie Curie | Sahel J.A.,French National Center for Scientific Research | Sahel J.A.,Rothschild | And 5 more authors.
Journal of Clinical Investigation | Year: 2014

Aniridia is a panocular disorder that severely affects vision in early life. Most cases are caused by dominantly inherited mutations or deletions of the PAX6 gene, which encodes a transcription factor that is essential for the development of the eye and the central nervous system. In this issue of the JCI, Gregory- Evans and colleagues demonstrate that early postnatal topical administration of an ataluren-based formulation reverses congenital malformations in the postnatal mouse eye, providing evidence that manipulation of PAX6 after birth may lead to corrective tissue remodeling. These findings offer hope that ataluren administration could be a therapeutic paradigm applicable to some major congenital eye defects.


Bendali A.,French Institute of Health and Medical Research | Bendali A.,Paris-Sorbonne University | Bendali A.,French National Center for Scientific Research | Bouguelia S.,CNRS Structure and Properties of Molecular Architectures Laboratory | And 20 more authors.
Analyst | Year: 2014

Direct interfacing of neurons with electronic devices has been investigated for both prosthetic and neuro-computing applications. In vitro neuronal networks provide great tools not only for improving neuroprostheses but also to take advantage of their computing abilities. However, it is often difficult to organize neuronal networks according to specific cell distributions. Our aim was to develop a cell-type specific immobilization of neurons on individual electrodes to produce organized in vitro neuronal networks on multi-electrode arrays (MEAs). We demonstrate the selective capture of retinal neurons on antibody functionalized surfaces following the formation of self-assembled monolayers from protein-thiol conjugates by simple contact and protein-polypyrrole deposits by electrochemical functionalization. This neuronal selection was achieved on gold for either cone photoreceptors or retinal ganglion neurons using a PNA lectin or a Thy1 antibody, respectively. Anti-fouling of un-functionalized gold surfaces was optimized to increase the capture efficiencies. The technique was extended to electrode arrays by addressing electropolymerization of pyrrole monomers and pyrrole-protein conjugates to active electrodes. Retinal ganglion cell recording on the array further demonstrated the integrity of these neurons following their selection on polypyrrole-coated electrodes. Therefore, this protein-polypyrrole electrodeposition could provide a new approach to generate organized in vitro neuronal networks. © 2014 The Royal Society of Chemistry.


Bendali A.,French Institute of Health and Medical Research | Bendali A.,Paris-Sorbonne University | Bendali A.,French National Center for Scientific Research | Agnes C.,CEA Saclay Nuclear Research Center | And 19 more authors.
PLoS ONE | Year: 2014

Direct electrode/neuron interfacing is a key challenge to achieve high resolution of neuronal stimulation required for visual prostheses. Neuronal interfacing on biomaterials commonly requires the presence of glial cells and/or protein coating. Nanocrystalline diamond is a highly mechanically stable biomaterial with a remarkably large potential window for the electrical stimulation of tissues. Using adult retinal cell cultures from rats, we found that glial cells and retinal neurons grew equally well on glass and nanocrystalline diamond. The use of a protein coating increased cell survival, particularly for glial cells. However, bipolar neurons appeared to grow even in direct contact with bare diamond. We investigated whether the presence of glial cells contributed to this direct neuron/diamond interface, by using purified adult retinal ganglion cells to seed diamond and glass surfaces with and without protein coatings. Surprisingly, these fully differentiated spiking neurons survived better on nanocrystalline diamond without any protein coating. This greater survival was indicated by larger cell numbers and the presence of longer neurites. When a protein pattern was drawn on diamond, neurons did not grow preferentially on the coated area, by contrast to their behavior on a patterned glass. This study highlights the interesting biocompatibility properties of nanocrystalline diamond, allowing direct neuronal interfacing, whereas a protein coating was required for glial cell growth. © 2014 Bendali et al.


Cwerman-Thibault H.,French Institute of Health and Medical Research | Cwerman-Thibault H.,Paris-Sorbonne University | Cwerman-Thibault H.,French National Center for Scientific Research | Augustin S.,French Institute of Health and Medical Research | And 14 more authors.
Comptes Rendus - Biologies | Year: 2014

Mitochondrial disorders cannot be ignored anymore in most medical disciplines; indeed their minimum estimated prevalence is superior to 1 in 5000 births. Despite the progress made in the last 25 years on the identification of gene mutations causing mitochondrial pathologies, only slow progress was made towards their effective treatments. Ocular involvement is a frequent feature in mitochondrial diseases and corresponds to severe and irreversible visual handicap due to retinal neuron loss and optic atrophy. Interestingly, three clinical trials for Leber Congenital Amaurosis due to RPE65 mutations are ongoing since 2007. Overall, the feasibility and safety of ocular Adeno-Associated Virus delivery in adult and younger patients and consistent visual function improvements have been demonstrated. The success of gene-replacement therapy for RPE65 opens the way for the development of similar approaches for a broad range of eye disorders, including those with mitochondrial etiology such as Leber Hereditary Optic Neuropathy (LHON). © 2013 Académie des sciences.


Froger N.,Institute National Of La Sante Et Of La Recherche Medicale Umr 968 | Froger N.,University Pierre and Marie Curie | Froger N.,French National Center for Scientific Research | Cadetti L.,Institute National Of La Sante Et Of La Recherche Medicale Umr 968 | And 56 more authors.
PLoS ONE | Year: 2012

Retinal ganglion cell (RGC) degeneration occurs in numerous retinal diseases leading to blindness, either as a primary process like in glaucoma, or secondary to photoreceptor loss. However, no commercial drug is yet directly targeting RGCs for their neuroprotection. In the 70s, taurine, a small sulfonic acid provided by nutrition, was found to be essential for the survival of photoreceptors, but this dependence was not related to any retinal disease. More recently, taurine deprivation was incriminated in the retinal toxicity of an antiepileptic drug. We demonstrate here that taurine can improve RGC survival in culture or in different animal models of RGC degeneration. Taurine effect on RGC survival was assessed in vitro on primary pure RCG cultures under serum-deprivation conditions, and on NMDA-treated retinal explants from adult rats. In vivo, taurine was administered through the drinking water in two glaucomatous animal models (DBA/2J mice and rats with vein occlusion) and in a model of Retinitis pigmentosa with secondary RGC degeneration (P23H rats). After a 6-day incubation, 1 mM taurine significantly enhanced RGCs survival (+68%), whereas control RGCs were cultured in a taurine-free medium, containing all natural amino-acids. This effect was found to rely on taurine-uptake by RGCs. Furthermore taurine (1 mM) partly prevented NMDA-induced RGC excitotoxicity. Finally, taurine supplementation increased RGC densities both in DBA/2J mice, in rats with vein occlusion and in P23H rats by contrast to controls drinking taurine-free water. This study indicates that enriched taurine nutrition can directly promote RGC survival through RGC intracellular pathways. It provides evidence that taurine can positively interfere with retinal degenerative diseases. © 2012 Froger et al.


Guillaumont R.,French Academy of science | Lipkowski J.,Polish Academy of Sciences | Petelenz B.,Polish Academy of Sciences | Vairon J.-P.,University Pierre and Marie Curie
Journal of Chemical Education | Year: 2013

The events organized for IYC 2011 were held in tandem with MSC100, that is, the joint French-Polish celebrations marking the centenary of the awarding of the Nobel Prize for Chemistry to Marie Skłodowska-Curie. These celebrations emphasized the traditional cultural bonds that exist between the two countries, the unique contribution of Marie and Pierre Curie to the development of science, and the beneficial role of Marie Skłodowska- Curie's discoveries. This communication summarizes one of the invited papers to the ConfChem online conference A Virtual Colloquium to Sustain and Celebrate IYC 2011 Initiatives in Global Chemical Education, held from May 18 to June 28, 2012, and jointly hosted by the ACS DivCHED Committee on Computers in Chemical Education and the IUPAC Committee on Chemistry Education. © 2013 The American Chemical Society and Division of Chemical Education, Inc.

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