April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Calbindin D28k Is Sole Calcium Binding Protein With Neuroprotective Function Against Pressure-Induced Retinal Ischemia-Reperfusion in Rats
Author Affiliations & Notes
  • S. Kim
    Department of Anatomy, The Catholic University of Korea, Seoul, Republic of Korea
  • J. Cha
    Department of Anatomy, The Catholic University of Korea, Seoul, Republic of Korea
  • J. Jeon
    Department of Anatomy, The Catholic University of Korea, Seoul, Republic of Korea
  • M.-H. Chun
    Department of Anatomy, The Catholic University of Korea, Seoul, Republic of Korea
  • I.-B. Kim
    Department of Anatomy, The Catholic University of Korea, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships  S. Kim, None; J. Cha, None; J. Jeon, None; M.-H. Chun, None; I.-B. Kim, None.
  • Footnotes
    Support  Korean Research Foundation Grant (KRF 2007-313-E00007), Medical Research Center Grant (R13-2002-005-01002-9)
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 123. doi:
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      S. Kim, J. Cha, J. Jeon, M.-H. Chun, I.-B. Kim; Calbindin D28k Is Sole Calcium Binding Protein With Neuroprotective Function Against Pressure-Induced Retinal Ischemia-Reperfusion in Rats. Invest. Ophthalmol. Vis. Sci. 2009;50(13):123.

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

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Abstract

Purpose: : Excessive calcium is thought to be a critical step in various neurodegenerative processes including ischemia. Calbindin D28k (CB), parvalbumin (PV) and calretinin (CR) which belong to the EF-hand calcium-binding protein family are implicated to have neuroprotective role to various pathologic conditions by buffering the excessive calcium. However, it still has not been clear that these proteins have the neuroprotective function. We have examined whether three calcium binding proteins play neuroprotective role against ischemic injury in the retina.

Methods: : The expression of CB, PV and CR in the ischemic rat retina induced by increasing intraocular pressure was investigated at protein level, by using western blot analysis and immunocytochemistry.

Results: : Retinas affected by ischemia became progressively thinner with increasing reperfusion time after the ischemic insult due to a loss of retinal cells in the inner and outer nuclear layers. CB was strongly expressed in the horizontal cells in both normal and affected retinas, and the density of the horizontal cells was not changed. PV was mainly expressed in AII amacrine cells of the normal rat retina, while in the affected retina PV was expressed in a type of cone bipolar cells possibly connecting with AII amacrine cells via gap junctions. The density of AII amacrine cell type was decreased. CR was strongly expressed in several kinds of amacrine, ganglion, and displaced amacrine cells in both normal and affected retinas. The expression pattern was changed and the cell density was markedly decreased in ischemic retinas. Protein levels of CB throughout the ischemic retinas showed no large changes, while those of PV and CR in ischemic retinas were significantly decreased by the passage of time after ischemic injury.

Conclusions: : These results suggest that among three calcium binding proteins only CB may have a protective function to ischemic insult by their ability to buffer calcium influx in the rat retina.

Keywords: ischemia • neuroprotection • calcium 
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