A novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress

Please use this identifier to cite or link to this item: http://hdl.handle.net/10045/13049
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dc.contributorNeurobiología del Sistema Visual y Terapia Génica de Enfermedades Neurodegenerativasen
dc.contributor.authorKehat, Rinat-
dc.contributor.authorZemel, Esther-
dc.contributor.authorCuenca, Nicolás-
dc.contributor.authorEvron, Tama-
dc.contributor.authorToiber, Debra-
dc.contributor.authorLoewenstein, Anat-
dc.contributor.authorSoreq, Hermona-
dc.contributor.authorPerlman, Ido-
dc.contributor.otherUniversidad de Alicante. Departamento de Biotecnologíaen
dc.date.accessioned2010-01-20T12:45:01Z-
dc.date.available2010-01-20T12:45:01Z-
dc.date.issued2007-03-
dc.identifier.citationKEHAT, Rinat, et al. “A novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress". Investigative Ophthalmology and Visual Science. Vol. 48, No. 3 (Mar. 2007). ISSN 0146-0404, pp. 1290-1297en
dc.identifier.issn0146-0404 (Print)-
dc.identifier.issn1552-5783 (Online)-
dc.identifier.urihttp://hdl.handle.net/10045/13049-
dc.description.abstractPURPOSE: To study the involvement of stress-induced acetylcholinesterase (AChE) expression in light-induced retinal damage in albino rats. METHODS: Adult albino rats were exposed for 24 hours to bright, damaging light. AChE expression was monitored by in situ hybridization, by histochemistry for AChE activity, and by immunocytochemistry. An orphan antisense agent (Monarsen; Ester Neurosciences, Ltd., Herzlia Pituach, Israel) was administered intraperitoneally to minimize light-induced AChE expression. The electroretinogram (ERG) was recorded to assess retinal function. RESULTS: Twenty-four-hour exposure to bright light caused severe reduction in the ERG responses and augmented expression of mRNA for the "read-through" variant of AChE (AChE-R) in photoreceptor inner segments (IS), bipolar cells, and ganglion cells. AChE activity increased in IS. The expressed AChE protein was a novel variant, characterized by an extended N terminus (N-AChE). Systemic administration of the orphan antisense agent, Monarsen, reduced the photic induction of mRNA for AChE-R, and of the N-AChE protein. Rats exposed to bright, damaging light and treated daily with Monarsen exhibited larger ERG responses, relatively thicker outer nuclear layer (ONL), and more ONL nuclei than did rats exposed to the same damaging light but treated daily with saline. CONCLUSIONS: The findings indicate that the photic-induced novel variant of AChE (N-AChE-R) may be causally involved with retinal light damage and suggest the use of RNA targeting for limiting such damage.en
dc.description.sponsorshipSupported in part by the Chief Scientist, Israel Ministry of Health, the Selma Mitrani Age Related Macular Degeneration Research Fund (IP), and the European Alternative Splicing Network of Excellence Grant EURASNET LSH-2004-1.1.5-3 (HS).en
dc.languageengen
dc.publisherAssociation for Research in Vision and Ophthalmologyen
dc.subjectAcetylcholinesteraseen
dc.subjectCell deathen
dc.subjectPhotoreceptor cellsen
dc.subjectRetinal degenerationen
dc.subject.otherOftalmologíaen
dc.titleA novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stressen
dc.typeinfo:eu-repo/semantics/articleen
dc.peerreviewedsien
dc.identifier.doi10.1167/iovs.06-0847-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
Appears in Collections:INV - NEUROVIS - Artículos de Revistas

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