September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
The role of TAF-9 in a rat model of anterior ischemic optic neuropathy after recombinant human granulocyte colony stimulating factor treatment.
Author Affiliations & Notes
  • CHIN-TE HUANG
    Department of Ophthalmology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan
    Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan
  • YAO-TSENG WENG
    Institute of Eye Research, Buddhist Tzu Chi General Hospital, Hualien, Taiwan
  • Rong-Kung Tsai
    Institute of Eye Research, Buddhist Tzu Chi General Hospital, Hualien, Taiwan
    Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan
  • Footnotes
    Commercial Relationships   CHIN-TE HUANG, None; YAO-TSENG WENG, None; Rong-Kung Tsai, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5080. doi:
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      CHIN-TE HUANG, YAO-TSENG WENG, Rong-Kung Tsai; The role of TAF-9 in a rat model of anterior ischemic optic neuropathy after recombinant human granulocyte colony stimulating factor treatment.. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5080.

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

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Abstract

Purpose : Non-arteritic anterior ischemic optic neuropathy (NAION) is the most common acute optic neuropathy in patients over 50 years of age and most probably results from flow impairment to the anterior optic nerve, which generates optic nerve (ON) ischemia. We tested the probable mechanism of granulocyte colony-stimulating factor (G-CSF) treatment in the rat model of anterior ischemic optic neuropathy (rAION) to rescue retinal ganglion cells (RGCs).

Methods : Our previous report demonstrated that immediate administration of recombinant human G-CSF had neuroprotective effects in a rAION model through the dual actions of anti-inflammation and anti-apoptosis. In order to investigate the mechanism of anti-apoptosis, we compared RNA expression patterns between rAION-inducted rats and rAION-inducted rats with G-CSF treatment on 7 day after rAION induction by using microRNA expression array. We also confirmed the RNA expression by using real time RT-PCR and confirmed the protein expression by using western blotting.

Results : According to microRNA array analysis, we found that 476 genes were induced and 113 genes were reduced by G-CSF treatment in the rAION model. One G-CSF induced protein, TAF9, was confirmed that RNA expression was increased 3.8-fold and protein expression was increased 2.5-fold in the G-CSF treated group. To investigate the role of TAF9, we evaluated anti-apoptotic effect of G-CSF treatment, G-CSF plus TAF9 siRNA treatment, G-CSF plus scramble siRNA treatment, and PBS treatment in the hypoxic retinal pigmented epithelium (RPE) injury model. We found that inhibition of TAF9 expression can reduce the protective effect of G-CSF in the hypoxic RPE injury model.

Conclusions : The expected findings provide much crucial information about neuroprotective effect of the G-CSF-induced TAF9 in response to ischemic stress in the rAION model.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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