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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Title: A novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress
Authors: Kehat, Rinat | Zemel, Esther | Cuenca, Nicolás | Evron, Tama | Toiber, Debra | Loewenstein, Anat | Soreq, Hermona | Perlman, Ido
Research Group/s: Neurobiología del Sistema Visual y Terapia Génica de Enfermedades Neurodegenerativas
Center, Department or Service: Universidad de Alicante. Departamento de Biotecnología
Keywords: Acetylcholinesterase | Cell death | Photoreceptor cells | Retinal degeneration
Knowledge Area: Oftalmología
Issue Date: Mar-2007
Publisher: Association for Research in Vision and Ophthalmology
Citation: 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
Abstract: 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.
Sponsor: 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
Language: eng
Type: info:eu-repo/semantics/article
Peer Review: si
Appears in Collections:INV - NEUROVIS - Artículos de Revistas

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