March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Retinal Ganglion Cell Degeneration In The Senescence-accelerated Mouse
Author Affiliations & Notes
  • Yasunari Munemasa
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Yasushi Kitaoka
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Kaori Kojima
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Satoki Ueno
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Footnotes
    Commercial Relationships  Yasunari Munemasa, None; Yasushi Kitaoka, None; Kaori Kojima, None; Satoki Ueno, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 778. doi:
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    • Get Citation

      Yasunari Munemasa, Yasushi Kitaoka, Kaori Kojima, Satoki Ueno; Retinal Ganglion Cell Degeneration In The Senescence-accelerated Mouse. Invest. Ophthalmol. Vis. Sci. 2012;53(14):778.

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

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Abstract

Purpose: : The senescence-accelerated mouse (SAM) has been established as a model of accelerated aging. SAM consists of the senescence-accelerated prone mouse (SAMP) and senescence-accelerated resistant mouse (SAMR), which exhibits normal aging process. We previously showed that the neural cell in the RGCL of SAM P8 and P10 retina was more vulnerable than SAMR retina against ONC.In the present study, we investigated the change of retinal ganglion cell (RGC) and Sirtuin 1 (Sirt1), which is a member of the sirtuin family of proteins and related with aging process, in SAMR, SAMP8, and SAMP10.

Methods: : Three month male SAMR, SAMP8, and SAMP10 were used in this study. Intraocular pressure (IOP) measurement was performed with a portable tonometer in the awake state. RGC was labeled by placing gel foam soaked in 6% solution of fluorogold at the superior colliculus. RGC number was counted at three fields in each retinal quadrant with fluorescence microscope. Morphological analysis of the inner nuclear layer (INL) and the outer nuclear layer (ONL) was performed with hematoxylin eosin (HE) stain with retinal transverse sections. The number of cells in the INL and the ONL was counted in the area at 1.0-1.5 mm from optic disc. The change of Sirt1 in the retina was studied with immunohistochemistry (IHC) and immunoblot (IB).

Results: : No significant difference of IOP measurement was observed in SAMR, SAMP8, and SAMP10. The number of RGCs in SAMR, SAMP8, and SAMP10 were 3571.549, 1921.858, and 1916.213 (/ mm2), respectively. RGC in SAMP8 and P10 was significantly decreased, compared with those in SAMR. No significant changes in the INL and the ONL were observed in SAMR, SAMP8, and SAMP10. IB showed that a significant decrease in Sirt1 was observed in the retinas of SAMP8 and SAMP10, compared to SAMR. An abundant Sirt1 was seen in the RGC and the IPL of SAMR retina, compared to those in SAMP8 and SAMP10.

Conclusions: : Morphological analysis indicated that RGC degeneration was observed in SAMP8 and SAMP10 retinas, compared to SAMR. A decrease in Sirt1 of SAMP8 and SAMP10 was involved in the process of RGC degeneration.

Keywords: retina • aging • retinal degenerations: cell biology 
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