{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T13:05:58Z","timestamp":1782219958767,"version":"3.54.5"},"reference-count":67,"publisher":"MDPI AG","issue":"3","license":[{"start":{"date-parts":[[2024,1,23]],"date-time":"2024-01-23T00:00:00Z","timestamp":1705968000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIH","award":["RO1 EY015304"],"award-info":[{"award-number":["RO1 EY015304"]}]},{"name":"NIH","award":["R01NS087632"],"award-info":[{"award-number":["R01NS087632"]}]},{"name":"Hillside Foundation","award":["RO1 EY015304"],"award-info":[{"award-number":["RO1 EY015304"]}]},{"name":"Hillside Foundation","award":["R01NS087632"],"award-info":[{"award-number":["R01NS087632"]}]},{"name":"NIH","award":["RO1 EY015304"],"award-info":[{"award-number":["RO1 EY015304"]}]},{"name":"NIH","award":["R01NS087632"],"award-info":[{"award-number":["R01NS087632"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>We evaluated whether inhibiting sterile alpha and (Toll\/interleukin receptor (TIR)) motif-containing 1 (SARM1) activity protects retinal ganglion cells (RGCs) following ischemic axonopathy (rodent nonarteritic anterior ischemic optic neuropathy: rNAION) by itself and combined with ciliary neurotrophic factor (CNTF). Genetically modified SARM1(\u2212) rats were rNAION-induced in one eye and compared against equivalently induced wild-type animals of the same background. Optic nerve (ON) diameters were quantified using optical coherence tomography (SD-OCT). RGCs were quantified 30 d post-induction using retinal stereology for Brn3a(+) nuclei. ON sections were analyzed by TEM and immunohistochemistry. SARM1(\u2212)(\u2212) and WT animals were then bilaterally sequentially rNAION-induced. One eye received intravitreal vehicle injection following induction; the contralateral side received CNTF and was analyzed 30 d post-induction. Inhibiting SARM1 activity suppressed axonal collapse following ischemic axonopathy. SARM1(\u2212) animals significantly reduced RGC loss, compared with WT animals (49.4 \u00b1 6.8% RGC loss in SARM1(\u2212) vs. 63.6 \u00b1 3.2% sem RGC loss in WT; Mann\u2013Whitney one-tailed U-test, (p = 0.049)). IVT-CNTF treatment vs. IVT-vehicle in SARM1(\u2212) animals further reduced RGC loss by 24% at 30 d post-induction, but CNTF did not, by itself, improve long-term RGC survival in WT animals compared with vehicle (Mann\u2013Whitney one-tailed t-test; p = 0.033). While inhibiting SARM1 activity is itself neuroprotective, combining SARM1 inhibition and CNTF treatment generated a long-term, synergistic neuroprotective effect in ischemic neuropathy. Combinatorial treatments for NAION utilizing independent neuroprotective mechanisms may thus provide a greater effect than individual treatment modalities.<\/jats:p>","DOI":"10.3390\/cells13030202","type":"journal-article","created":{"date-parts":[[2024,1,23]],"date-time":"2024-01-23T04:17:40Z","timestamp":1705983460000},"page":"202","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Synergistic Protection of Retinal Ganglion Cells (RGCs) by SARM1 Inactivation with CNTF in a Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy"],"prefix":"10.3390","volume":"13","author":[{"given":"Yan","family":"Guo","sequence":"first","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zara","family":"Mehrabian","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey","family":"Milbrandt","sequence":"additional","affiliation":[{"name":"Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA"},{"name":"Needleman Center for Neurometabolism and Axonal Therapeutics, St. Louis, MO 63110, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron","family":"DiAntonio","sequence":"additional","affiliation":[{"name":"Needleman Center for Neurometabolism and Axonal Therapeutics, St. Louis, MO 63110, USA"},{"name":"Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7758-0136","authenticated-orcid":false,"given":"Steven L.","family":"Bernstein","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA"},{"name":"Anatomy and Neurobiology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,1,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"994","DOI":"10.1016\/j.jocn.2009.04.002","article-title":"Non-arteritic anterior ischaemic optic neuropathy: A review and update","volume":"16","author":"Kerr","year":"2009","journal-title":"J. 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