September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Increased expression of osteopontin in retinal degeneration induced by blue-light-emitting diode exposure in mice
Author Affiliations & Notes
  • SuJin Park
    Dept. of Anatomy, The Catholic University of Korea, Seoul, Korea (the Republic of)
  • Seung Wook Chang
    Dept. of Anatomy, The Catholic University of Korea, Seoul, Korea (the Republic of)
  • Gyu Hyun Kim
    Dept. of Anatomy, The Catholic University of Korea, Seoul, Korea (the Republic of)
  • Sun-Sook Paik
    Dept. of Anatomy, The Catholic University of Korea, Seoul, Korea (the Republic of)
  • Hyung Il Kim
    Gyeongju St. Mary's Eye Clinic, Gyeongju-si, Korea (the Republic of)
  • In-Beom Kim
    Dept. of Anatomy, The Catholic University of Korea, Seoul, Korea (the Republic of)
    Catholic Neuroscience Institute, Seoul, Korea (the Republic of)
  • Footnotes
    Commercial Relationships   SuJin Park, None; Seung Wook Chang, None; Gyu Hyun Kim, None; Sun-Sook Paik, None; Hyung Il Kim, None; In-Beom Kim, None
  • Footnotes
    Support  Basic Science Research Program through the NRF of Korea #2013R1A2A2A01014070
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 6537. doi:
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      SuJin Park, Seung Wook Chang, Gyu Hyun Kim, Sun-Sook Paik, Hyung Il Kim, In-Beom Kim; Increased expression of osteopontin in retinal degeneration induced by blue-light-emitting diode exposure in mice. Invest. Ophthalmol. Vis. Sci. 2016;57(12):6537.

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

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Abstract

Purpose : Osteopontin (OPN) is a multifunctional adhesive glycoprotein implicated in a variety of proinflammatory as well as neuroprotective and repair-promoting effects in the brain pathophysiology. In this study, as a first step to understand the role of OPN in retinal degeneration (RD), we examined changes in OPN expression in a mouse RD model induced by a blue light-emitting diode (LED) exposure.

Methods : RD was induced in BALB/c mice by exposure to a blue LED (460 nm) for 2 hours. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Immunohiscothcemistry with anti-OPN was performed and compared to that with anti-glial fibrillary acidic protein (GFAP), a commonly used marker for retinal stress condition including inflammation.

Results : OPN expression in RD retinas was markedly increased at 24 h after blue LED, sustained by 72 h, and subsided at 120 h. Increased expression of OPN was found in microglial cells located in the outer nuclear layer (ONL), the outer plxiform layer (OPL), and the subretinal space where inner and outer segments of photoreceptors are located. This expression was restricted to central retina in which photoreceptor cell death occurred. Interestingly, all OPN in the ONL and the OPL, and some OPN plaques in subretinal space were closely associated with microglia, while most of OPN plaques in subretinal space were not. In addition, OPN was more acutely and legion-specifically expressed than GFAP.

Conclusions : These results indicate that OPN could be a useful marker for retinal stress or injury and might acts as a proinflammatory factor produced by microglia and a phagocytosis-inducing opsonin by binding mitochondiria or cell membrane in debris of photoreceptor outer and inner segments in RD retinas, suggesting that OPN plays an important role in RD pathogenesis.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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