May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
NPD1 Promotes Survival of Retinal Ganglion Cells Following Optic Nerve Transection
Author Affiliations & Notes
  • Q. Qin
    New York Medical College, Valhalla, NY
    Cell Biology and Anatomy,
  • K.A. Patil
    New York Medical College, Valhalla, NY
  • K. Gronert
    New York Medical College, Valhalla, NY
  • S.C. Sharma
    New York Medical College, Valhalla, NY
    Ophthalmology, Cell Biology and Anatomy,
  • Footnotes
    Commercial Relationships  Q. Qin, None; K.A. Patil, None; K. Gronert, None; S.C. Sharma, None.
  • Footnotes
    Support  NIH EY11295 (SCS) and NIH EY 016136 (KG)
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 4822. doi:
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      Q. Qin, K.A. Patil, K. Gronert, S.C. Sharma; NPD1 Promotes Survival of Retinal Ganglion Cells Following Optic Nerve Transection . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4822.

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

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Purpose: : Retinal ganglion cells (RGCs) in the mammalian retina degenerate and apoptotically die following Optic Nerve Transection (ONT) in a predictable, time–dependent manner. Docosahexanoic acid derived lipid mediator Neuroprotectin D1 (NPD1) is endogenously generated in the eye and the brain. NPD1 exhibits both anti–inflammatory and neuroprotective bioactivity. The later is of particular interest as NPD1 inhibits oxidative stress induced apoptosis in retinal pigment epithelium (RPE) cells and reduces mitochondrial damage in ischemia/reperfusion–induced infarcts. Present experiments were undertaken to evaluate the therapeutic potential of NPD1 and its biosynthetic pathway, to impede the progress of retinal ganglion cell (RGC) apoptosis, following optic never transection.

Methods: : Retinal ganglion cells were bilaterally prelabelled with Fluorogold (FG) five days before optic nerve transaction (ONT). NPD1 (5 µg) was dissolved in 200µl Hank’s buffer and the treatment was initiated by tail vein. Thirty minutes after the NPD1 injection, ONT was performed in right eye and the left eye of the animal was used as normal control. NPD1 was injected every alternate day after ONT and the rats were sacrificed on day 14. The number of FG–labelled RGCs from the flat–mounted retina was counted in both eyes. Endogenous formation of NPD1 in retinas of rats, 15–lipoxygenase (Alox15) deficient mice and their matched congenic C57BL/6J mice was analyzed by HPLC/GC/MS. mRNA expression of Alox15 was quantified by fluorescence–based kinetic PCR analyses.

Results: : NPD1 is generated in the retina and in vivo genetic deletion of Alox15 abrogates its biosynthesis. Systemic treatment with NPD1 was associated with significant protection against RGCs apoptosis. The percentage of RGCs in NPD1 treated group was 30% at 2 weeks after ONT. There was statistical significance comparing it to 12% of RGC survival in the ONT group without treatment (P<0.0001).

Conclusions: : These results provide evidence that NPD1 acts as a neuroprotectant to RGCs following ONT. Systemic treatment with NPD1 significantly protected RGCs following ONT. Collectively, these findings suggesting that NPD1 formation in the retina and its therapeutic amplification provide a potential target for suppressing RGCs apoptosis that is associated with retinal diseases.

Keywords: apoptosis/cell death • neuroprotection • lipids 

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