학술논문
A Potential Role of Crystallin in the Vitreous Bodies of Rats after Ischemia-reperfusion Injury
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- 영문명
- 발행기관
- 대한안과학회
- 저자명
- Seong Min Hong Yun Sik Yang
- 간행물 정보
- 『The Korean Journal of Ophthalmology』Vol.26 No.4, 248~254쪽, 전체 7쪽
- 주제분류
- 의약학 > 기타의약학
- 파일형태
- 발행일자
- 2012.08.30
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국문 초록
영문 초록
Purpose: Ischemia-reperfusion injury (I/R injury) is known not only to induce hypoxic and oxidative stress, but
also to cause retinal degeneration in rats. Crystallins, known to inhibit the formation of reactive oxygen species,
reduce apoptotic cell death. Our goal was to clarify not only the role of I/R injury-mediated crystallins, but
also to evaluate the correlation of these compounds to anti-inflammation in the vitreous body.
Methods: Twenty-four Sprague-Dawley rats were used in this study. We induced I/R injury by clamping the optic
nerve for 30 minutes and then releasing it. The vitreous bodies were obtained from the experimental and
control subjects 24, 48, and 72 hours after I/R injury. Two-dimensional electrophoresis was performed, and
the targeted spots were further investigated using matrix-assisted laser desorption-ionization time-of-flight
mass spectrometry, spectrophotometry, Western blotting, and histological examination.
Results: After I/R injury, 23 spots were identified as crystallins. The ßB2 crystallins were transcriptionally and
post-translationally regulated, whereas the αB crystallins were controlled by post-translational modifications
in the vitreous bodies of the rats. The total amounts of αA and ß crystallins (including isotypes of ß crystalline)
had increased 48 hours after injury. The phosphorylation of αB crystallin (at serine residues 19, 45, and 59)
was significantly increased 48 hours later, whereas phosphorylation of ERK1/2 showed the greatest decrease.
Conclusions: During hypoxic and oxidation stress, our results suggest that phosphorylated αB crystalline inhibits
RAS, resulting in the inactivation of ERK1/2. The phosphorylation of αB crystallin may be associated with
the inflammatory suppression in the vitreous body via the I/R injury model system.
목차
Materials and Methods
Results
Discussion
Conflict of Interest
Acknowledgements
References
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