April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Membrane bound Flt-1 protects against optic nerve degeneration in nerve crush injury in rats
Author Affiliations & Notes
  • Zhao Hongwei
    The 306th hospital of PLA, BeiJing, China
  • Hironori Uehara
    Moran Eye Center, Salt Lake, UT
  • Ling Luo
    The 306th hospital of PLA, BeiJing, China
  • Chuang Nie
    The 306th hospital of PLA, BeiJing, China
  • Alex Jones
    Moran Eye Center, Salt Lake, UT
  • Balamurali Ambati
    Moran Eye Center, Salt Lake, UT
  • Xiaohui Zhang
    Moran Eye Center, Salt Lake, UT
  • Hu Lianna
    The 306th hospital of PLA, BeiJing, China
  • Qiu Changyu
    The 306th hospital of PLA, BeiJing, China
  • Footnotes
    Commercial Relationships Zhao Hongwei, None; Hironori Uehara, None; Ling Luo, None; Chuang Nie, None; Alex Jones, None; Balamurali Ambati, None; Xiaohui Zhang, None; Hu Lianna, None; Qiu Changyu, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5737. doi:https://doi.org/
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      Zhao Hongwei, Hironori Uehara, Ling Luo, Chuang Nie, Alex Jones, Balamurali Ambati, Xiaohui Zhang, Hu Lianna, Qiu Changyu; Membrane bound Flt-1 protects against optic nerve degeneration in nerve crush injury in rats. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5737. doi: https://doi.org/.

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

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Abstract

Purpose: In recent years, VEGF-B has been shown to be a potent neuroprotective factor and an apoptosis inhibitor, rather than an angiogenic factor.VEGF-B deficiency exacerbated retinal ganglion cell death.VEGF-B increased the number of surviving retinal ganglion cells via its receptor (Flt-1) in rat optic nerve injury.Flt-1 has two isoforms: membrane-bound form (mFlt-1) and soluble form(sFlt-1). Recently, we demonstrated that sFlt-1, as an anti-angiogenic factor, strongly protect photoreceptor avascularity. In this study, we explored whether either the soluble or membrane isoform of Flt-1 could protect against optic nerve degeneration.

Methods: To establish a rat model of optic nerve damage,adult female 200-250g Spraque-Dawley rats was exposed through a supraorbital approach and crushed bilaterally within the orbit, 2 mm from the eye, using forceps as described previously.Retinal ganglion cells (RGC), inner/outer nuclear cells degeneration was determined by TUNEL staining and immunohistochemistry. The levels of sFlt-1 and mFlt-1 were detected by RT-PCR and Western Blot at 6 hr, 24hr, 3 day, 7 day, and 21 day after injury. Intravitreal injection with mFlt-1 or sFlt-1 plasmid was performed at 24 hr after injury. RGC and inner/outer nuclear cells apoptosis and degeneration evaluation was repeated at day 21 after intervention.

Results: The level of mFlt increased dramatically at 6 hr after injury, peaked at 48th hour, gradually reduced after a week. Comparably, the level of sFlt-1 barely changed at each time point. RGC and inner/outer nuclear cells apoptosis and degeneration were much lower in mFlt-1 treatment group than that of sFlt-1treatment group.

Conclusions: mFlt-1, but not soluble was able to promote RGC preservation after optic nerve injury.

Keywords: 629 optic nerve • 656 protective mechanisms  
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