April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Intravenously Administrated Anti-Recoverin Antibody Does Not Pass Through Blood Retinal Barrier
Author Affiliations & Notes
  • K. Kim
    Seoul National University College of Medicine, Seoul, Republic of Korea
  • J. Kim
    Fight against Angiogenesis-Related Blindness Laboratory, Department of Ophthalmology, Seoul National University College of Medicine & Seoul Artificial Eye Center, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
  • K. Kim
    NeuroVascular Coordination Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea
  • Y. Yu
    Fight against Angiogenesis-Related Blindness Laboratory, Department of Ophthalmology, Seoul National University College of Medicine & Seoul Artificial Eye Center, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
  • J. Kim
    Fight against Angiogenesis-Related Blindness Laboratory, Department of Ophthalmology, Seoul National University College of Medicine & Seoul Artificial Eye Center, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships  K. Kim, None; J. Kim, None; K. Kim, None; Y. Yu, None; J. Kim, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 837. doi:
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    • Get Citation

      K. Kim, J. Kim, K. Kim, Y. Yu, J. Kim; Intravenously Administrated Anti-Recoverin Antibody Does Not Pass Through Blood Retinal Barrier. Invest. Ophthalmol. Vis. Sci. 2010;51(13):837.

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

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Abstract

Purpose: : To investigate whether intravenously administrated anti-recoverin antibodies could pass through blood-retinal barrier (BRB) and lead to retinal cell death.

Methods: : The anti-recoverin antibody was intravenously injected via tail vein and the eye was enucleated after 1 day and 7 days. To induce BRB disruption, vascular endothelial growth factor (VEGF) was injected into the intravitreal cavity, which was confirmed by fluorescein angiography with fluorescein-conjugated dextran. Immunofluorescence staining for recoverin, CD31 and glial fibrillary acidic protein (GFAP) as well as TUNEL was performed. Western blot analysis for occluding and ZO-1/2 was performed.

Results: : Intravenously administrated anti-recoverin antibodies were exclusively distributed on retinal vessels which were co-localized with CD31, and led to neither increase of GFAP expression, as an indicator of retinal stress, nor apoptotic retinal cell death. Moreover, even in the condition of VEGF-induced BRB breakdown, anti-recoverin antibodies could not migrate across BRB and still remained on retinal vessels without retinal cytotoxicity.

Conclusions: : Our results suggest that high titer of intravascular anti-recoverin antibodies could not penetrate into the retina by themselves, and BRB breakdown mediated by dysregulation of tight junction might not be sufficient to allow anti-recoverin antibodies to pass through BRB.

Keywords: retina • autoimmune disease • CAR 
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