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Jpn J Ophthalmol. 2008 Mar-Apr;52(2):84-90. doi: 10.1007/s10384-007-0507-5. Epub 2008 Apr 30.

Proteomic analysis of rat retina in a steroid-induced ocular hypertension model: potential vulnerability to oxidative stress.

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1
Department of Ophthalmology and Visual Sciences, School of Medicine, University of the Ryukyus, Okinawa, Japan.

Abstract

PURPOSE:

To investigate global protein expression profiles in the retinas of normal and glucocorticoid-induced ocular hypertensive rats by proteomic analysis.

METHODS:

Ocular hypertension was induced by topical application of dexamethasone (DEX) for 4 weeks. Age-matched untreated rats served as controls. Intraocular pressure (IOP) was monitored by an electronic tonometer. Retinal protein expression profiling was carried out by two-dimensional fluorescence difference gel electrophoresis (2-D DIGE). Proteins were identified by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry.

RESULTS:

In DEX-treated rats, average IOP was elevated significantly compared with controls. With DEX treatment, levels of four proteins were altered, as revealed by 2-D DIGE and MALDI-TOF mass spectrometry: apolipoprotein A1 (apoA1), a lipid-binding protein, upregulated 1.9-fold, P < 0.05; alpha A crystallin (CRYAA), a molecular chaperone, downregulated 2.7-fold, P < 0.01; superoxide dismutase 1 (SOD1), an antioxidant enzyme, downregulated 2.3-fold, P < 0.05; and triosephosphate isomerase 1 (TPI1), a glycolytic enzyme, downregulated 2.3-fold, P < 0.01.

CONCLUSIONS:

Downregulation of CRYAA, SOD1, and TPI1, observed here after a short period of DEX-induced ocular hypertension, may be involved in the onset of neural damage in steroid-induced glaucoma.

PMID:
18626730
DOI:
10.1007/s10384-007-0507-5
[Indexed for MEDLINE]
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