April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Suppression of Retinal Neovascularization by Anti-CCR3 Treatment for Oxygen Induced Retinopathy Model in Mice
Author Affiliations & Notes
  • Shuichiro Hirahara
    Ophthalmology, Nagoya City University, Nagoya, Japan
  • Miho Nozaki
    Ophthalmology, Nagoya City University, Nagoya, Japan
  • Masaharu Ohbayashi
    Ophthalmology, Nagoya City University, Nagoya, Japan
  • Norio Hasegawa
    Ophthalmology, Nagoya City University, Nagoya, Japan
  • Daisuke Ozone
    Ophthalmology, Nagoya City University, Nagoya, Japan
  • Yuichiro Ogura
    Ophthalmology, Nagoya City University, Nagoya, Japan
  • Footnotes
    Commercial Relationships Shuichiro Hirahara, None; Miho Nozaki, None; Masaharu Ohbayashi, None; Norio Hasegawa, None; Daisuke Ozone, None; Yuichiro Ogura, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5402. doi:
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      Shuichiro Hirahara, Miho Nozaki, Masaharu Ohbayashi, Norio Hasegawa, Daisuke Ozone, Yuichiro Ogura; Suppression of Retinal Neovascularization by Anti-CCR3 Treatment for Oxygen Induced Retinopathy Model in Mice. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5402.

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

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Abstract

Purpose: To investigate the association between retinal neovascularization and CCR3 and to evaluate the efficacy of anti-CCR3 treatment for retinal neovascularization in mice model of oxygen induced retinopathy (OIR).

Methods: Retinal neovascularization model was obtained by OIR model in C57BL/6J mice. The anti-CCR3 antibody was injected into vitreous humor at postnatal day12, when the pups were taken out from the oxygen chamber. The area of capillary non-perfusion was measured by retinal whole mount. ELISA was performed to evaluate the chronological change of CCL11 (eotaxin) expression in retina. Real-time RT-PCR for CCR3 expression in the retina, and immunohistochemistry for CCR3, CCL11,CD31 and Ki67 was examined.

Results: Intravitreous injection of anti-CCR3 antibody significantly suppressed the area of capillary non-perfusion (p<0.05) in retina of OIR model mice. The mean CCL11 protein level was temporally decreased under hyperoxia (p<0.05).In the retina of OIR, the CCL11 level began to rise at postnatal day14, significantly increased at postnatal day17 (P17) (p<0.05). CCR3 mRNA expression was significantly upregulated in P17 OIR murine retina. Intravitreous injection of anti-CCR3 antibody appeared to suppress CCR3, CCL11 and Ki67 expression in retina of OIR model mice.

Conclusions: There was correlation between retinal neovascularization between CCR3 and retinal neovascularization. The present data suggest that the anti-CCR3 treatment can suppress retinal neovascularization. Although our findings may warrant further investigation, anti-CCR3 treatment may have potential as a new therapy for proliferative retinopathy such as diabetic retinopathy and retinopathy of prematurity.

Keywords: 635 oxygen • 700 retinal neovascularization • 749 vascular occlusion/vascular occlusive disease  
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