Lens-specific regulation of the thioredoxin-1 gene, but not thioredoxin-2, upon in vivo photochemical oxidative stress in the Emory mouse.
Autor: | Reddy PG; Membrane Biochemistry Laboratory, Department of Ophthalmology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA., Bhuyan DK, Bhuyan KC |
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Jazyk: | angličtina |
Zdroj: | Biochemical and biophysical research communications [Biochem Biophys Res Commun] 1999 Nov 19; Vol. 265 (2), pp. 345-9. |
DOI: | 10.1006/bbrc.1999.1691 |
Abstrakt: | Thioredoxin (TRX)-1 and TRX-2 redox-regulatory genes were analyzed in the lens and some other tissues of the Emory mouse, a model for age-related human cataract. The cDNA transcripts of mRNAs encoding TRX-1 and TRX-2 genes were isolated and cloned by RT-PCR from the lens, liver, kidney, and tail, and the cDNA sequences were similar to the reported sequences of murine TRX-1 and TRX-2 genes. In vivo photochemical oxidative stress to the Emory mice resulted in fivefold upregulation of the lens TRX-1 gene at 3 weeks and declined thereafter. Western blot analysis revealed a fourfold increase of TRX-1 protein in the lens at 3 weeks after oxidative stress. The TRX-2 gene in the lens was not changed up to 5 weeks and decreased by 50% thereafter. However, the expressions of these genes in the liver, kidney, and tail were not changed. Fluorescent light or riboflavin alone did not affect the expressions of TRX-1 and TRX-2 genes in the lens. Thus, we show the expressions of TRX-1 and TRX-2 genes in the lens, liver, kidney, and tail and lens-specific upregulation of the TRX-1 gene and protein expressions, possibly as a protective response to the altered redox state of the lens after in vivo oxidative stress to the Emory mouse. (Copyright 1999 Academic Press.) |
Databáze: | MEDLINE |
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