June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Inflammatory infiltrates in hyperoxia-induced proliferative retinopathy in C57BL/6J and C57BL/6N strains
Author Affiliations & Notes
  • Michelle Lajko
    Ophthalmology, Northwestern University, Chicago, Illinois, United States
  • Herminio Joey Cardona
    Pediatrics, Northwestern University, Chicago, Illinois, United States
  • Joann M. Taylor
    Pediatrics, Northwestern University, Chicago, Illinois, United States
  • Kathryn N Farrow
    Pediatrics, Northwestern University, Chicago, Illinois, United States
  • Amani A Fawzi
    Ophthalmology, Northwestern University, Chicago, Illinois, United States
  • Footnotes
    Commercial Relationships   Michelle Lajko, None; Herminio Cardona, None; Joann Taylor, None; Kathryn Farrow, None; Amani Fawzi, None
  • Footnotes
    Support  NIH Grant R21HD077336
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 3461. doi:
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    • Get Citation

      Michelle Lajko, Herminio Joey Cardona, Joann M. Taylor, Kathryn N Farrow, Amani A Fawzi; Inflammatory infiltrates in hyperoxia-induced proliferative retinopathy in C57BL/6J and C57BL/6N strains. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3461.

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

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Abstract

Purpose : In hyperoxia-induced proliferative retinopathy (HIPR), the retina had disrupted vascular development, disorganized angiogenesis, and retinal detachment. We wanted to characterize the differences in inflammatory markers in two strains of mice in HIPR.

Methods : We used the HIPR model to compare C57BL/6J and C57BL/6N strains. In HIPR, mice were exposed to 75% oxygen from birth to post-natal day (P) 14. Mice were euthanized at P14 or recovered in room air for one day (P15), one week (P21), or two weeks (P28). Room air controls were euthanized at the same time points. In retinal cross sections, we immunostained for vascular endothelium (Isolectin B4, IB4), macrophages (F4/80), microglia (Iba-1), and lymphocytes (CD45R).

Results : Both strains in HIPR had disrupted blood vessel development and angiogenesis in the inner plexiform layer at P21 and P28. In room air controls, Iba-1 stained the resident microglia in the inner nuclear layers. For both strains in HIPR, Iba-1 staining was mainly observed at P21 in the inner plexiform layer and retinal ganglion cell layer, decreasing by P28. In room air controls, there was no F4/80 or CD45R staining at any time point. In, contrast, HIPR in both strains showed F4/80 and CD45R stained cells in the inner plexiform layer and retinal ganglion cell layer by P28. There were no cells positively stained for F4/80 or CD45 in either strain at P14-P21 in HIPR.

Conclusions : Microglia migrated to the inner retina at the site of angiogenesis by P21, followed by macrophages and lymphocytes P28 in both strains in HIPR. We did not observe any strain differences, considering the location of the infiltrates or the time points at which these cells appeared.

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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