May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
AQP9 Changes in Expression Upon Insults and Unique Localization to Mitochondria in Retinal Ganglion Cells
Author Affiliations & Notes
  • M.-H. Yang
    Univ of North Texas HSC, Fort Worth, Texas
  • A. Dibas
    Univ of North Texas HSC, Fort Worth, Texas
  • J. Bobich
    Chemistry, Texas Christian University, Fort Worth, Texas
  • T. Yorio
    Univ of North Texas HSC, Fort Worth, Texas
  • Footnotes
    Commercial Relationships M. Yang, None; A. Dibas, None; J. Bobich, None; T. Yorio, None.
  • Footnotes
    Support The glaucoma foundation
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4177. doi:
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      M.-H. Yang, A. Dibas, J. Bobich, T. Yorio; AQP9 Changes in Expression Upon Insults and Unique Localization to Mitochondria in Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4177.

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

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Purpose:: The water channel, aquaporin9 (AQP9) is enriched in selected neuronal populations and is unique in its ability to act as a lactate-glycerol channel supplying neurons with alternative fuel under ischemic conditions especially due to its expression in the mitochondria. Therefore, its expression may alter under various insults inflicted on retinal ganglion cells (RGCs). The purpose of the study was to examine AQP9 expression in RGCs under conditions of elevated intraocular pressure (IOP) and following intravitreal injection of endothelin.

Methods:: Insults on retinal ganglion cells were induced by elevation of intraocular pressure in rat eyes or via intravitreal injection of endothelin. Immunohistochemistry using a combination of thy-1/aquaporin-9 antibodies was used to follow changes in the retinal ganglion cell layer. Real-time PCR was used for measuring changes in AQP9 and beta-actin. Also, changes in AQP9 were followed in total retinal extracts using Western blotting and in vitro following hypoxic conditions with isolated RGC-5 cells.

Results:: Intravitreal injection of ET resulted in reduction of AQP9 as determined by RT-PCR after 48hr. Similar reduction was observed in total retinal extracts after 72hrs. By contrast, optic nerve head astrocytes showed enormous up-regulation of AQP9 that co-localized with GFAP. However, changes in AQP9 in the Morrison model rats gave contradictory changes showing increases or decreases in retinas of different animal as determined by RT-PCR. Such changes did reflect different IOP differences between animals. Interestingly, AQP9 was localized to mitochondria in RGC-5 cells and its expression increased upon insults such as hypoxia.

Conclusions:: Changes in AQP9 expression may be correlated with extent of cellular injuries in retinal ganglion cells suggesting a novel role in retinal ganglion cellular death upon elevation of intraocular pressure.

Keywords: ganglion cells • intraocular pressure • ischemia 

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