SOD2 knockdown mouse model of early AMD.

SOD2 knockdown mouse model of early AMD. Research Abstract Details 

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SOD2 knockdown mouse model of early AMD. Abstract Text:

Verline Justilien,Ji-Jing Pang,Kutralanathan Renganathan,Xianquan Zhan,John W Crabb,So Ra Kim,Janet R Sparrow,William W Hauswirth,Alfred S Lewin,

PURPOSE: To test the hypothesis that oxidative injury to the retinal pigment epithelium (RPE) may lead to retinal damage similar to that associated with the early stages of age-related macular degeneration (AMD). METHODS: A ribozyme that targets the protective enzyme manganese superoxide dismutase (MnSOD) was expressed in RPE-J cells, and adeno-associated virus (AAV) expressing the ribozyme gene was injected beneath the retinas of adult C57BL/6 mice. The RPE/choroid complex was examined for SOD2 protein levels and protein markers of oxidative damage using immunoblot analysis and LC MS/MS-identification of proteins and nitration sites. Lipids were extracted from retinal tissue and analyzed for the bis-retinoid compounds A2E and iso-A2E. The mice were analyzed by full-field electroretinography (ERG) for light response. Light and electron microscopy were used to measure cytological changes in the retinas. RESULTS: The treatment of RPE-J cells with Rz432 resulted in decreased MnSOD mRNA and protein as well as increased levels of superoxide anion and apoptotic cell death. When delivered by AAV, Rz432 reduced MnSOD protein and increased markers of oxidative damage, including nitrated and carboxyethylpyrrole-modified proteins in the RPE-choroid of mice. Ribozyme delivery caused a progressive loss of electroretinograph response, vacuolization, degeneration of the RPE, thickening of Bruch's membrane, and shortening and disorganization of the photoreceptor outer and inner segments. Progressive thinning of the photoreceptor outer nuclear layer resulted from apoptotic cell death. Similar to the eyes of patients with AMD, ribozyme-treated eyes exhibited increased autofluorescence and elevated levels of A2E and iso-A2E, major bis-retinoid pigments of lipofuscin. CONCLUSIONS: These results support the hypothesis that oxidative damage to the RPE may play a role in some of the key features of AMD.

SOD2 knockdown mouse model of early AMD. Publishing Authors By Initials

V Justilien,JJ Pang,K Renganathan,X Zhan,JW Crabb,SR Kim,JR Sparrow,WW Hauswirth,AS Lewin,

For similar investigative techniques: chemistry, analytical: mass spectrometry: tandem mass spectrometry research abstracts see: investigative techniques: chemistry, analytical: mass spectrometry: tandem mass spectrometry research

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SOD2 knockdown mouse model of early AMD. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Investigative ophthalmology & visual science

VOLUME: 48

Page Numbers: 4407-20

Journal Abbreviation: Invest. Ophthalmol. Vis. Sci.

ISSN: 0146-0404

DAY: 3

MONTH: Oct

YEAR: 2007

SOD2 knockdown mouse model of early AMD. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7703701

SOD2 knockdown mouse model of early AMD. Keywords Mesh Terms:

KEYWORDS: Tandem Mass Spectrometry

MESH TERMS: metabolism

Chemical & Substance for Abstract: SOD2 knockdown mouse model of early AMD. Information

Substance Name: superoxide dismutase 2

Registry Number: EC 1.15.1.1

Grant and Affiliation Information for SOD2 knockdown mouse model of early AMD.

AFFILIATION: Department of Molecular Genetics, University of Florida, Gainesville, Florida, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS36302

ACRONYM: NS

MEDLINETA: Invest Ophthalmol Vis Sci

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