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Brain Res. 2013 Oct 9;1534:76-86. doi: 10.1016/j.brainres.2013.07.053. Epub 2013 Aug 21.

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

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  • 1Wilmer Eye Institute, The Johns Hopkins Hospitals, Baltimore, MD 21287, USA; Farabi Eye Hospital, Tehran University of Medical Science, Tehran, Iran. Electronic address:


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.


Axonal regeneration; Inflammation; Ischemic optic neuropathy; RhoA

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