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2002 Fiscal Year Final Research Report Summary

Apoptosis cascade in hyperoxia-induced photoreceptor cell death.

Research Project

Project/Area Number 13671858
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Ophthalmology
Research InstitutionKansai Medical University

Principal Investigator

MATSUMURA Miyo  Kansai Medical University, Faculty of Medicine, Professor, 医学部, 教授 (30144380)

Co-Investigator(Kenkyū-buntansha) YAMADA Haruhiko  Kansai Medical University, Faculty of Medicine, Instructor, 医学部, 助手 (50288841)
Project Period (FY) 2001 – 2002
Keywordshyperoxia / apoptosis / retinal cell / Ocaspase
Research Abstract

Purpose: Hyperoxia causes vascular endothelial cell and photoreceptor cell dropout in the mouse retina. We previously demonstrated that hyperoxic photorecepter cell death started from around day 5 of oxigen exposure and peaked on day 7. Our purpose in this study is to investigate the mechanisms by which these cells die from hyperoxic stress in vivo.
Method: C57bl/6j mice were exposed to a 75% concentration of oxygen for 1, 2 or 3 weeks. At each time point the mice were sacrificed and enucleated. Retinas were isolated from the eye balls, homogenized , and processed for protein isolation. To quantitate the protein levels of each apoptosis associated proteins, we performed Western blotting using antibodies of FAS, FAS-L, Bax, Bcl-2, Caspase 3, 8, and Caspase 9. To investigate the role of Fas and Fas-L proteins in this apoptosis pathway, we exposed FAS knockout mouse and FAS-L knokuout mouse under hyperoxic condition and quantitate the TUNEL index from their retinal sections.
Results: Western blotting revealed upregulation of Caspase 3 and Bax in the retinas after one week exposure in hyperoxia. FAS knockout mouse and FAS-L knockout mouse exposed to hyperoxia showed no difference of the TUNEL index compared to wild type mouse control.
Conclusion: The mechanisms by which apoptosis occurs in photoreceptor cells death is still unclear, but upregulation of Bax may play a key role in this apoptosis cascade. FAS and FAS-L are unlikely to involve in photoreceptor apoptosis from hyperoxia.

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Published: 2004-04-14  

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