RhoA activity and post-ischemic inflammation in an experimental model of adult rodent anterior ischemic optic neuropathy

Abstract Activation of inflammatory cells and the RhoA signaling pathway may contribute to optic nerve damage following non-arteritic anterior ischemic optic neuropathy (NAION). We induced an optic nerve infarct with a photothrombotic mechanism in a rat model of AION (rAION). Immunohistochemistry an...

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Bibliographic Details
Published in:Brain research 2013-10, Vol.1534, p.76-86
Main Authors: Fard, Masoud Aghsaei, Ebrahimi, Katayoon Baradaran, Miller, Neil R
Format: Article
Language:English
Subjects:
adults
animal models
Animals
Axonal regeneration
Biological and medical sciences
brain
Disease Models, Animal
eyes
ganglia
immunohistochemistry
infarction
Inflammation
Ischemic optic neuropathy
Medical sciences
Microglia - metabolism
Miscellaneous
Nerve Regeneration
nerve tissue
Neurology
Ophthalmology
Optic Neuropathy, Ischemic - metabolism
Optic Neuropathy, Ischemic - pathology
peripheral nervous system diseases
Rats
Retinal Ganglion Cells - pathology
Retinal Ganglion Cells - physiology
Retinitis - metabolism
rho-Associated Kinases - metabolism
RhoA
rhoA GTP-Binding Protein - metabolism
rodents
signal transduction
stroke
Stroke - metabolism
Stroke - pathology
Western blotting
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Summary:Abstract Activation of inflammatory cells and the RhoA signaling pathway may contribute to optic nerve damage following non-arteritic anterior ischemic optic neuropathy (NAION). We induced an optic nerve infarct with a photothrombotic mechanism in a rat model of AION (rAION). Immunohistochemistry and Western blot were performed to detect activation of RhoA signaling and inflammation. The extent of Rho activity, inflammation, retinal ganglion cell (RGC) loss and extent of axon regeneration were determined at 8 and 14 days after infarct. Eight days after stroke, we observed significant inflammation and RhoA activity at the site of infarction as well as loss of cells in the RGC layer. RhoA activity had decreased and inflammation had decreased at day 14 compared with day 8; however, loss of RGCs was greater at 14 days than at 8 days. Stroked eyes showed minor axon regeneration around the optic nerve lesion site at both 8 and 14 days. These results demonstrate that inflammation and RhoA activation occur in rAION at the site of infarction.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2013.07.053