May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
GCSF rescues retinal cell apoptosis in transient optic ischemia in the rat
Author Affiliations & Notes
  • S.–P. Huang
    Department of Ophthalmology and Visual Science, Washington University School of Medicine, St. Louis, MO
    Department of Ophthalmology, Taipei Veterans General Hospital, Taipei, Taiwan Republic of China
  • C.–N. Khor
    School of Medicine, Fu–Jen Catholic University, Taipei, Taiwan Republic of China
  • S.–M. Lee
    Department of Ophthalmology, Taipei Veterans General Hospital, Taipei, Taiwan Republic of China
  • C.–Y. Ke
    School of Medicine, Fu–Jen Catholic University, Taipei, Taiwan Republic of China
  • H. Li
    Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan Republic of China
  • Y.–J. Lee
    School of Medicine, Fu–Jen Catholic University, Taipei, Taiwan Republic of China
  • Footnotes
    Commercial Relationships  S. Huang, None; C. Khor, None; S. Lee, None; C. Ke, None; H. Li, None; Y. Lee, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 3284. doi:
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      S.–P. Huang, C.–N. Khor, S.–M. Lee, C.–Y. Ke, H. Li, Y.–J. Lee; GCSF rescues retinal cell apoptosis in transient optic ischemia in the rat . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3284.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To investigate the effect of GCSF in protecting retinal cell apoptosis in transient optic ligation–ischemia animal model. Methods: Male SD rats, 150–250 g, were used in this study. Optic arterial ligation was performed on one eye of the animal. In experimental groups, GCSF was given to the rats for five days after the optic ligation. In shame–operative group, GCSF was replaced with normal saline after the same operation. Some other animals received no treatment after the optic ligation for studying the retinal change after the operation. The contralateral eyes of the same animal were left untreated as control. The animals were also injected with BrdU during the time of observation. After two–week observation, the animals were scarified, and both experimental eyes and control eyes were collected individually for investigation. For histological observation, HE staining was used for morphological study on retinae of the eyes. The cell numbers of INL and ONL were also counted. Specific cell markers for ganglion cells and photoreceptors were used to identify the retinal cell types. Immunocytochemistry for BrdU was used to label the process of cell proliferation. PCR was used to detect the gene expression in the retinal cells from different treatments. Results: The histological study of the retinae and the retinal cell count showed that the transient optic arterial ligation made cell loss in retina two weeks after the operation. Animals received GCSF showed more retinal cells survived in the operated eye, compared to the shame–operative animals. Results of PCR also showed that the retinal gene expression, such as opsin and Thy–1, decreased after the optic ligation. Administration of GCSF reversed the decrease of retinal gene expression in the operated eyes after the optic ligation. GCSF may perform a neuroprotective effect as preventing cell loss in the retina. Conclusions: GCSF prevents the cell apoptosis caused by optic arterial ligation in the rats. It is therefore that GCSF provides a possible therapeutic effect in optic stroke or ischemia.

Keywords: retina • cell death/apoptosis • neuroprotection 
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