June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Optic Nerve as a Source of Retinal Mononuclear Cells Post-Injury
Author Affiliations & Notes
  • Dale S Gregerson
    Ophthalmology & Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, United States
  • Neal D Heuss
    Ophthalmology & Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, United States
  • Mark Pierson
    Ophthalmology & Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, United States
  • Scott W McPherson
    Ophthalmology & Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, United States
  • Footnotes
    Commercial Relationships   Dale Gregerson, None; Neal Heuss, None; Mark Pierson, None; Scott McPherson, None
  • Footnotes
    Support  1 R01 EY025209-01A1; RPB, Inc.; Minnesota Lions Clubs; Wallin Neuroscience Discovery Fund
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5744. doi:
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    • Get Citation

      Dale S Gregerson, Neal D Heuss, Mark Pierson, Scott W McPherson; Optic Nerve as a Source of Retinal Mononuclear Cells Post-Injury. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5744.

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

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Abstract

Purpose : We previously found mononuclear cells in murine CNS tissues, including retina, that expressed GFP from a transgenic CD11c promoter. Their origin is of interest. Their frequency was elevated in retina following several types of stress or injury or inflammation, and they possessed the ability to process and present antigen to naïve antigen-specific T cells in vivo.

Methods : Retinal ganglion cells in adult mice were injured in one of three procedures; an ON crush, a partial ON transection, and a full ON transection; all procedures spared the ophthalmic artery to preserve retinal circulation. ON injuries were done in CD11c-GFP mice, in beta-actin GFP parabiotic mice, in mice with tamoxifen-induced depletion of CX3CR1+ cells, and in radiation bone marrow chimeras, to further examine the origins of the responding GFPhi cells. ON and retina were collected for analysis by immunofluorescence and flow cytometry.

Results : The origin of GFPhi cells in CD11c-GFP mice depended on the injury. Of particular interest was the observation that full ON transection (artery was spared) gave a limited GFPhi cell response relative to an ONC (p<0.05) or partial transection (p<0.05), despite the injury of a much larger number of ganglion cell axons following a full transection. All ON injuries led to appearance of a significant number of cells with Ki67+ nuclei, while few cells in retina post-ONC were Ki67+. The significance of the small number of Ki67+ cells in ONC retina was further examined by comparison with retinas inflamed by experimental autoimmune uveoretinitis. Inflamed retinas had many Ki67+ cells including T lymphocytes, CD11b+ cells and GFPhi cells. ON injury in parabiotic mice gave no evidence of recruitment from the circulation (p<0.01). ON injury in tamoxifen-depleted mice induced a small mononuclear cell response that was largely GFPhi (p<0.05). The large mononuclear cell response in the ON post-injury may lead to migration of cells from the ON into retina, following the severed axons.

Conclusions : While Ki67+ cells were found in injured ON, Tam-depletion substantially delayed the retinal response to the ON injury. Precursors of GFPhi cells may be more prevalent or active in the ON, and contribute to the GFPhi cells found associated with RGC and nerve fibers post-ON injury. The reduced yield of retinal GFPhi cells after a full ON transection may reflect macrophage migration along injured axons, lost following a full transection.

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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