IOVS Arteriosclerosis, Thrombosis, and Vascular Biology
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Originally published In Press as doi:10.1167/iovs.08-1716 on April 25, 2008
 (Investigative Ophthalmology and Visual Science. 2008;49:3535-3543.)
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-1716
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Protective Effect of Thioredoxins 1 and 2 in Retinal Ganglion Cells after Optic Nerve Transection and Oxidative Stress

Yasunari Munemasa,1,2 Seok Hwan Kim,1 Jae Hong Ahn,1 Jacky M. K. Kwong,1 Joseph Caprioli,1,3 and Natik Piri1,3

1From the Jules Stein Eye Institute and the 3Brain Research Institute, University of California at Los Angeles, Los Angeles, California; and the 2Department of Ophthalmology, St. Marianna University School of Medicine, Kawasakishi, Japan.

PURPOSE. Oxidative stress has been implicated in retinal ganglion cell (RGC) death pathways after optic nerve transection (ONT) and during glaucomatous neuropathy. The authors investigated the expression and cell-protective roles of thioredoxins (cytosolic Trx1 and mitochondrial Trx2), important regulators of the cellular redox state, on RGCs after ONT and pharmacologic oxidative stress induction.

METHODS. ONT was performed on adult Wistar rats. Trx1 and Trx2 quantitative and spatial expression were examined with Western blot and immunohistochemistry, respectively. Electroporation and calcium phosphate-mediated procedures were used to deliver Trx1 and Trx2 expression constructs to RGCs in vivo and to cultured RGC-5 cells, respectively. Cell-protective effects of Trx1 and Trx2 overexpression on RGCs after ONT and on RGC-5 cells treated with glutamate/buthionine sulfoximine (BSO) were determined by RGC density analysis and cell viability assay, respectively.

RESULTS. Upregulation of Trx1 and Trx2 was observed in RGCs at different times after ONT and in RGC-5 cells after glutamate/BSO treatment. Trx1 and Trx2 overexpression in RGC-5 cells increased their survival rate by approximately twofold and threefold 24 and 48 hours after glutamate/BSO treatment, respectively. A neuroprotective effect of Trx1 and Trx2 overexpression on RGCs was also observed in vivo; the survival rate of RGCs was increased by 35% and 135%, respectively, 1 and 2 weeks after ONT.

CONCLUSIONS. These findings provide evidence for in vitro and in vivo cell-protective effects of Trx1 and Trx2 on RGCs against oxidative stress–induced neurodegeneration.






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