A novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress

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Títol: A novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress
Autors: Kehat, Rinat | Zemel, Esther | Cuenca, Nicolás | Evron, Tama | Toiber, Debra | Loewenstein, Anat | Soreq, Hermona | Perlman, Ido
Grups d'investigació o GITE: Neurobiología del Sistema Visual y Terapia Génica de Enfermedades Neurodegenerativas
Centre, Departament o Servei: Universidad de Alicante. Departamento de Biotecnología
Paraules clau: Acetylcholinesterase | Cell death | Photoreceptor cells | Retinal degeneration
Àrees de coneixement: Oftalmología
Data de publicació: de març-2007
Editor: Association for Research in Vision and Ophthalmology
Citació bibliogràfica: KEHAT, 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. 1290-1297
Resum: PURPOSE: 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.
Patrocinadors: Supported 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).
URI: http://hdl.handle.net/10045/13049
ISSN: 0146-0404 (Print) | 1552-5783 (Online)
DOI: 10.1167/iovs.06-0847
Idioma: eng
Tipus: info:eu-repo/semantics/article
Revisió científica: si
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