June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
The granulocyte colony-stimulating factor (G-CSF) induced stabilization of blood-optic nerve barrier (BOB) in the optic nerve (ON) crush model via PI3K/AKT activation
Author Affiliations & Notes
  • Yao-Tseng Wen
    Buddhist Tzu Chi General Hospital, Hualien, Taiwan
  • Rong-Kung Tsai
    Buddhist Tzu Chi General Hospital, Hualien, Taiwan
  • Footnotes
    Commercial Relationships   Yao-Tseng Wen, None; Rong-Kung Tsai, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 1094. doi:
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      Yao-Tseng Wen, Rong-Kung Tsai; The granulocyte colony-stimulating factor (G-CSF) induced stabilization of blood-optic nerve barrier (BOB) in the optic nerve (ON) crush model via PI3K/AKT activation. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1094.

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

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Abstract

Purpose : The purpose of this study is to investigate why G-CSF can stabilize BOB in the ON crush model.

Methods : The ONs of adult male Wistar rats (150-180 g) were crushed by a standardized method. The control eyes received a sham operation. G-CSF, G-CSF plus AKT inhibitor, or phosphate-buffered saline (PBS control) was immediately administered after ON crush for 5 days by subcutaneous injection. Rats were euthanized at 1 or 2 weeks after the crush injury. RGC density was counted by retrograde labeling with FluoroGold application to the superior colliculus. TUNEL assay was used to measure the apoptotic RGCs in the RGC layer. BOB stabilization was evaluated by measuring Evans blue extravasation, IHC staining, and Western blot analysis of Claudin-3, ZO-1.

Results : Two weeks after the insult, the RGC densities in the central and mid-peripheral retinas in ON-crushed, G-CSF-treated rats were significantly higher than that of the G-CSF plus AKT inhibitor- or PBS-treated rats. TUNEL assays showed fewer apoptotic cells in the retinal sections in the PBS-treated group and G-CSF plus AKT-treated group. Macrophage infiltration analysis showed more ED-1 positive cells in the G-CSF treated group than the G-CSF plus AKT- or PBS-treated groups. Evans blue extravasation was demonstrated that AKT inhibitor can disrupt G-CSF induced BOB stabilization. Additionally, G-CSF stabilizes the BOB by up-regulating Claudins 3 and ZO-1 in the insulted ON.

Conclusions : We demonstrate G-CSF plays a pivotal role in attenuating neuroinflammation and BBB disruption via activation of the PI3K/Akt pathway in the ON crush model.

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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