May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
The Association Of Cullin–5 With Retinal Cell Death
Author Affiliations & Notes
  • M. Suzuki
    Hiroshima University, Hiroshima, Japan
  • S. Tanimoto
    Hiroshima University, Hiroshima, Japan
  • H. Okumichi
    Hiroshima University, Hiroshima, Japan
  • T. Ue
    Hiroshima University, Hiroshima, Japan
  • H. Tamura
    Hiroshima University, Hiroshima, Japan
  • H.K. Mishima
    Hiroshima University, Hiroshima, Japan
  • T. Kanamoto
    Hiroshima University, Hiroshima, Japan
  • Footnotes
    Commercial Relationships  M. Suzuki, None; S. Tanimoto, None; H. Okumichi, None; T. Ue, None; H. Tamura, None; H.K. Mishima, None; T. Kanamoto, None.
  • Footnotes
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Investigative Ophthalmology & Visual Science May 2006, Vol.47, 4814. doi:
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      M. Suzuki, S. Tanimoto, H. Okumichi, T. Ue, H. Tamura, H.K. Mishima, T. Kanamoto; The Association Of Cullin–5 With Retinal Cell Death . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4814.

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

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Abstract

Purpose: : In previous reports, the results of proteomics analysis of DBA2/J mouse, glaucoma model mouse, retina showed that the endogeneous protein expressions of Cullin–5 were up–regulated in nine months age. So, we intend to investigate the molecular and biological function of Cullin–5 on retinal ganglion cells (RGCs).

Methods: : Immunohistochemistry procedure was performed in C57BL mice retina to examine the localization of Cullin–5. RNA knock down of Cullin–5 was also performed on retinal cells with or without glutamate treatment, and analyzed the cell biological changes.

Results: : Endogeneous Cullin–5 were specifically expressed RGCs. Retinal cell death induced by glutamate was inhibited by RNA knock down of Cullin–5.

Conclusions: : Cullin–5 may play an important role on RGC death in glaucoma.

Keywords: ganglion cells 
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