ANALYSIS OF LOCALIZATION OF ADULT T-CELL LEUKEMIA-DERIVED FACTOR IN THE TRANSIENT ISCHEMIC RAT RETINA AFTER TREATMENT WITH OP-1206 ALPHA-CD, A PROSTAGLANDIN E(1) ANALOG

Citation
M. Yamamoto et al., ANALYSIS OF LOCALIZATION OF ADULT T-CELL LEUKEMIA-DERIVED FACTOR IN THE TRANSIENT ISCHEMIC RAT RETINA AFTER TREATMENT WITH OP-1206 ALPHA-CD, A PROSTAGLANDIN E(1) ANALOG, The Journal of histochemistry and cytochemistry, 45(1), 1997, pp. 63-70
Citations number
46
Categorie Soggetti
Cell Biology
ISSN journal
00221554
Volume
45
Issue
1
Year of publication
1997
Pages
63 - 70
Database
ISI
SICI code
0022-1554(1997)45:1<63:AOLOAT>2.0.ZU;2-V
Abstract
Prostaglandin E(1) (PGE(1)) is commonly used in therapy for obstructiv e diseases, including ischemic retinopathy, in which pathogenetic reac tive oxygen intermediates are responsible. However, the mechanism(s) o f PGE(1) in reducing tissue damage is still unclear. Adult T-cell leuk emia-derived factor/human thioredoxin (ADF) is induced by oxidative st resses and has protective activity against oxidative cellular injury. To evaluate the possible involvement of ADF in the tissue-protective e ffect of PGE(1), we analyzed ADF expression immunohistochemically usin g a rat transient retinal ischemia model. Rats were treated orally wit h 300 mu g/kg/day OP-1206 alpha-cyclodextrin clathrate (OP-1206), a st able PGE(1) analogue, for 14 days after photodynamic retinal vascular thrombosis by rose Bengal. Rats without any OP-1206 treatment were use d as controls. In the OP-1206-treated rats, minimal retinal atrophy du e to ischemia/reperfusion was observed histologically up to 14 days, w hereas in the non-treated rats the inner layer of the retina became ma rkedly atrophic. In parallel with the histological change, after 14 da ys following thrombosis ADF immunoreactivity was preserved on retinal pigment epithelial cells in the OP-1206-treated rats, whereas it was d iminished in the non-treated rats. These findings suggest an important role for ADF in the OP-1206-dependent suppression of retinal tissue d amage caused by oxidative insult.