July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Microglial regulation of inflammatory mediators following retinal detachment
Author Affiliations & Notes
  • Yoko Okunuki
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Steven Tabor
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Kip M Connor
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Yoko Okunuki, None; Steven Tabor, None; Kip Connor, None
  • Footnotes
    Support  R01EY027303
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 6604. doi:
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      Yoko Okunuki, Steven Tabor, Kip M Connor; Microglial regulation of inflammatory mediators following retinal detachment. Invest. Ophthalmol. Vis. Sci. 2019;60(9):6604.

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

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Purpose : We previously found that photoreceptor cell death was increased following retinal detachment (RD) in mice lacking microglia, suggesting that microglia have protective function in acute injury. Inflammatory factors produced by infiltrating inflammatory cells are suggested to be one of the worsening factors of photoreceptor cell death in RD. However, inflammatory cell infiltration was suppressed in the RD retina without microglia. In this study, we examined the levels of inflammatory factors in the RD retina with or without microglia in order to elucidate if alterations in inflammatory mediators is associated with the worsening of photoreceptor cell death observed in RD in mice lacking microglia.

Methods : Retinal microglia in C57BL/6 male mice were depleted with a Csf1r antagonist. RD was induced in the mice with microglia (control diet) or without microglia (Csf1r antagonist diet) (12 eyes/group). The retinas were isolated 24 hours after RD induction and retinal protein was extracted. Three retinas were pooled per sample (4 samples per group). 40 inflammatory factors in the retinal extracts were assessed using the Mouse Inflammation Antibody Array-Membrane (Abcam, ab133999).

Results : Among the 40 molecules assessed,12 molecules were expressed with more than 1.3 fold difference: GM-CSF (1.5 fold), RANTES (1.4 fold), SDF-1 (1.6 fold), IL-4 (1.4 fold), TNF-alpha (1.5 fold), IL-6 (1.4 fold), GCSF-1 (2.3 fold), and IL-12 p70 (1.4 fold) were increased, and IFN-g (0.6 fold), I-TAC (0.6 folds), CXCL1 (0.7 fold), and MIP-1 gamma (0.5 fold) were decreased in the RD retina lacking microglia.

Conclusions : A number of inflammatory factors were altered in the RD retina lacking retinal microglia: Of these 8 inflammatory factors were increased and 4 inflammatory factors were decreased. This result demonstrates that absence of microglia causes the imbalance of inflammatory factor levels after RD, which could lead to exacerbation of photoreceptor cell death. Further studies are needed to elucidate the role of these inflammatory mediators, their cellular source and contribution to the worsening phenotype in mice lacking retinal microglia.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.


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