Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/27750
Title: Enhanced survival of melanopsin-expressing retinal ganglion cells after injury is associated with the PI3 K/Akt pathway
Authors: Li, SY
Yau, SY
Chen, BY
Tay, DK
Lee, VWH
Pu, ML
Chan, HHL 
So, KF
Keywords: Glaucoma
Melanopsin
Optic nerve injury
Retinal ganglion cell
Issue Date: 2008
Publisher: Springer/Plenum Publishers
Source: Cellular and molecular neurobiology, 2008, v. 28, no. 8, p. 1095-1107 How to cite?
Journal: Cellular and Molecular Neurobiology 
Abstract: In the present study, we studied the factors that contribute to the injury-resistant property of melanopsin-expressing retinal ganglion cells (mRGCs). Since phosphatidylinositol-3 kinase (PI3 K)/Akt signaling pathway is one of the well-known pathways for neuronal cell survival, we investigated the survival of mRGCs by applying the PI3 K/Akt specific inhibitors after injury. Two injury models, unilateral optic nerve transection and ocular hypertension, were adopted using Sprague-Dawley rats. Inhibitors of PI3 K/Akt were injected intravitreally following injuries to inhibit the PI3 K/Akt signaling pathway. Retinas were dissected after designated survival time, immunohistochemistry was carried out to visualize the mRGCs using melanopsin antibody and the number of mRGCs was counted. Co-expression of melanopsin and phospho-Akt (pAkt) was also examined. Compared to the survival of non-melanopsin-expressing RGCs, mRGCs showed a marked resistance to injury and co-expressed pAkt. Application of PI3 K/Akt inhibitors decreased the survival of mRGCs after injury. Our previous study has shown that mRGC are less susceptible to injury following the induction of ocular hypertension. In this study, we report that mRGCs were injury-resistant to a more severe type of injury, the optic nerve transection. More importantly, the PI3 K/Akt pathway was found to play a role in maintaining the survival of mRGCs after injury.
URI: http://hdl.handle.net/10397/27750
DOI: 10.1007/s10571-008-9286-x
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