June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Effect of axonopathy on dynamics of acidic organelle in the axon of primary cultured retinal ganglion cells
Author Affiliations & Notes
  • Seiji Miyake
    Faculty of Medical Sciences, University of Fukui, Yoshida-gun, Fukui, Japan
  • Yuji Takihara
    Faculty of Medical Sciences, University of Fukui, Yoshida-gun, Fukui, Japan
    Cancer Science Institute of Singapore, National University of Singapore, Medical Drive, Singapore
  • Satoshi Yokota
    Graduate School of Medicine and Faculty of Medicine, Kyoto University, Kyoto, Japan
    Faculty of Medical Sciences, University of Fukui, Yoshida-gun, Fukui, Japan
  • Yoshihiro Takamura
    Faculty of Medical Sciences, University of Fukui, Yoshida-gun, Fukui, Japan
  • Masaru Inatani
    Faculty of Medical Sciences, University of Fukui, Yoshida-gun, Fukui, Japan
  • Footnotes
    Commercial Relationships   Seiji Miyake, None; Yuji Takihara, None; Satoshi Yokota, None; Yoshihiro Takamura, None; Masaru Inatani, None
  • Footnotes
    Support  MEXT 26893100 and 16K20311
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 2532. doi:
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      Seiji Miyake, Yuji Takihara, Satoshi Yokota, Yoshihiro Takamura, Masaru Inatani; Effect of axonopathy on dynamics of acidic organelle in the axon of primary cultured retinal ganglion cells. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2532.

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

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Abstract

Purpose : Glaucoma is characterized by the progressive loss of retinal ganglion cell (RGC) and its axon. However, molecular details of relationship between cell death and axonal degeneration remain poorly understood. We investigate the implication of dynamics of autophagy for RGC death under the axonal abnormality using live imaging in vitro.

Methods : RGCs were isolated from postnatal day 3 Sprague-Dawley rats by immunopanning method. After 7 days culture, acidic organelles were stained by LysoTracker. Dynamics were quantified from kymographs. To induce axonopathy, colchicine was used. Axonal transport of acidic organelles was observed at 5 time points: before, and at 6, 24, 72, and 120 hours after colchicine stimulation. Ethidium homodimer-1 (EthD-1) was used to detect cell viability.

Results : Property of axonal transport of 27 RGCs (n = 363) was classified into 4 categories; anterograde (1.4%), retrograde (90%), stationary (8.0%), and fluttering (0.28%). At 6 hours after induction of axonopathy for 14 (n = 236) of 27 RGCs, movement of almost acidic organelles were stationary. All acidic components were completely stopped 24 hours later. At 72 hours since giving stimulation, axonal fragmentation, and shrinking and disappearance of soma were observed in 71% of RGC. Finally, remaining RGCs were positive for EthD-1. In the control (13 of 27 RGCs), transport was kept for 120 hours and EthD-1 positive RGCs were not observed.

Conclusions : RGC death followed by cease of axonal transport. These results suggested that functional disorder of autophagy through axonal damage is one of the causes of glaucomatous optic neuropathy.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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