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The molecular signaling pathway leading from ocular hypertension to RGC degeneration, however, is not well defined. JNK signaling, a component of the mitogen-activated protein kinase (MAPK) family, and its canonical target, the transcription factor JUN, have been shown to regulate neurodegeneration in many different systems. JUN is expressed after glaucoma-relevant injuries and <jats:italic>Jun<\/jats:italic> deficiency protects RGCs after mechanical injury to the optic nerve. Here, we tested the importance of JNK\u2013JUN signaling for RGC death after ocular hypertensive axonal injury in an age-related, mouse model of ocular hypertension. Immunohistochemistry was performed to evaluate JUN expression in ocular hypertensive DBA\/2J mice. JUN was expressed in a temporal and spatial pattern consistent with a role in glaucomatous injury. To determine the importance of JUN in ocular hypertension-induced RGC death, a floxed allele of <jats:italic>Jun<\/jats:italic> and a retinal expressed cre recombinase (Six3-cre) were backcrossed onto the DBA\/2J background. Intraocular pressure (IOP) and gross morphology of the retina and optic nerve head were assessed to determine whether removing <jats:italic>Jun<\/jats:italic> from the developing retina altered IOP elevation or retinal development. <jats:italic>Jun<\/jats:italic> deficiency in the retina did not alter DBA\/2J IOP elevation or retinal development. Optic nerves and retinas were assessed at ages known to have glaucomatous damage in DBA\/2J mice. <jats:italic>Jun<\/jats:italic> deficiency protected RGC somas from ocular hypertensive injury, but did not protect RGC axons from glaucomatous neurodegeneration. <jats:italic>Jun<\/jats:italic> is a major regulator of RGC somal degeneration after glaucomatous ocular hypertensive injury. These results suggest in glaucomatous neurodegeneration, JNK\u2013JUN signaling has a major role as a pro-death signaling pathway between axonal injury and somal degeneration.<\/jats:p>","DOI":"10.1038\/cddis.2017.338","type":"journal-article","created":{"date-parts":[[2017,7,20]],"date-time":"2017-07-20T12:41:55Z","timestamp":1500554515000},"page":"e2945-e2945","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":59,"title":["JUN is important for ocular hypertension-induced retinal ganglion cell degeneration"],"prefix":"10.1038","volume":"8","author":[{"given":"Stephanie B","family":"Syc-Mazurek","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kimberly A","family":"Fernandes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2844-7632","authenticated-orcid":false,"given":"Richard T","family":"Libby","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,7,20]]},"reference":[{"key":"BFcddis2017338_CR1","doi-asserted-by":"publisher","first-page":"714","DOI":"10.1001\/archopht.120.6.714","volume":"120","author":"MO Gordon","year":"2002","unstructured":"Gordon MO, Beiser JA, Brandt JD, Heuer DK, Higginbotham EJ, Johnson CA et al. 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