Abstract
Purpose :
Optic neuritis and ischemic optic neuropathy are well known demyelinating optic neuropathies and NG2+ oligodendrocyte progenitor cells (OPCs) are believed to exert an important role in remyelination of demyelinating diseases. However, the changes in NG2+ OPC of the demyelinating neuropathies are still remains elusive. In this study, we aimed to investigate the temporal change of NG2+ OPC in the mouse models of demyelinating optic neuropathies.
Methods :
Using adult C57BL/6 mice, experimental autoimmune encephalomyelitis (EAE) model was induced with MOG35-55 peptide and ischemic ocular ischemic syndrome (OIS) model was made by unilateral common carotid artery occlusion. We analyzed the optic nerve histology of both models according to time course: acute and chronic phase. Demyelination was determined with Luxol fast blue staining. TUNEL assay and EdU cell proliferation assay were performed combined with immunofluorescence analysis of optic nerve.
Results :
Optic nerve of both EAE and OIS model showed demyelination. NG2+ OPCs were less ramified and depleted both in the optic nerve of acute and chronic EAE. In EAE, a positive correlation between the depletion of OPCs and the degree of demyelination was observed. A noticeable activation of OPCs were observed in acute OIS model and this change was associated with increased proliferation of OPC. However, in chronic OIS, the number of OPCs was decreased and their branches were shortened. Apoptotic OPC death was detected throughout acute and chronic phase of EAE model. On the other hand, in OIS model, OPC apoptosis was found only in the acute phase.
Conclusions :
Both optic neuritis and ischemic optic nerve insult accompany oligodendroglial injury: optic nerve demyelination. OPC changes are prominent throughout the time course of EAE. However, ischemic insult results in a phase dependent change in OPCs.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.