{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T13:46:47Z","timestamp":1791121607428,"version":"4.1.0"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2014,5,5]],"date-time":"2014-05-05T00:00:00Z","timestamp":1399248000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2014,9]]},"abstract":"<jats:p>Although axonal damage induces significant retinal ganglion cell (RGC) death, small numbers of RGCs are able to survive up to 7 days after optic nerve crush (NC) injury. To develop new treatments, we set out to identify patterns of change in the gene expression of axonal damage\u2010resistant RGCs. To compensate for the low density of RGCs in the retina, we performed retrograde labeling of these cells with 4Di\u201010ASP in adult mice and 7 days after NC purified the RGCs with fluorescence\u2010activated cell sorting. Gene expression in the cells was determined with a microarray, and the expression of <jats:italic>Ho\u20101<\/jats:italic> was determined with quantitative PCR (qPCR). Changes in protein expression were assessed with immunohistochemistry and immunoblotting. Additionally, the density of Fluoro\u2010gold\u2010labeled RGCs was counted in retinas from mice pretreated with CoPP, a potent HO\u20101 inducer. The microarray and qPCR analyses showed increased expression of <jats:italic>Ho\u20101<\/jats:italic> in the post\u2010NC RGCs. Immunohistochemistry also showed that HO\u20101\u2010positive cells were present in the ganglion cell layer (GCL), and cell counting showed that the proportion of HO\u20101\u2010positive cells in the GCL rose significantly after NC. Seven days after NC, the number of RGCs in the CoPP\u2010treated mice was significantly higher than in the control mice. Combined pretreatment with SnPP, an HO\u20101 inhibitor, suppressed the neuroprotective effect of CoPP. These results reflect changes in HO\u20101 activity to RGCs that are a key part of RGC survival. Upregulation of HO\u20101 signaling may therefore be a novel therapeutic strategy for glaucoma. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jnr.23398","type":"journal-article","created":{"date-parts":[[2014,5,5]],"date-time":"2014-05-05T15:20:30Z","timestamp":1399303230000},"page":"1134-1142","source":"Crossref","is-referenced-by-count":14,"title":["Critical neuroprotective roles of heme oxygenase\u20101 induction against axonal injury\u2010induced retinal ganglion cell death"],"prefix":"10.1002","volume":"92","author":[{"given":"Noriko","family":"Himori","sequence":"first","affiliation":[{"name":"Department of Ophthalmology Tohoku University Graduate School of Medicine  Miyagi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuichi","family":"Maruyama","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Tohoku University Graduate School of Medicine  Miyagi 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