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Dysregulated crosstalk between the vasculature and retinal neurons is increasingly recognized as a major factor contributing to the pathogenesis of vascular diseases. Class 3 semaphorins (SEMA3s), a group of neuron\u2010secreted axonal and vascular guidance factors, suppress pathological vascular growth in retinopathy. However, the upstream transcriptional regulators that mediate the function of SEMA3s in vascular growth are poorly understood. Here we showed that retinoic acid receptor\u2013related orphan receptor \u03b1 (ROR\u03b1), a nuclear receptor and transcription factor, is a novel transcriptional regulator of SEMA3E\u2010mediated neurovascular coupling in a mouse model of oxygen\u2010induced proliferative retinopathy. We found that genetic deficiency of ROR\u03b1 substantially induced\n                    <jats:italic>Sema3e<\/jats:italic>\n                    expression in retinopathy. Both ROR\u03b1 and SEMA3E were expressed in retinal ganglion cells. ROR\u03b1 directly bound to a specific ROR response element on the promoter of\n                    <jats:italic>Sema3e<\/jats:italic>\n                    and negatively regulated\n                    <jats:italic>Sema3e<\/jats:italic>\n                    promoter\u2013driven luciferase expression. Suppression of\n                    <jats:italic>Sema3e<\/jats:italic>\n                    using adeno\u2010associated virus 2 carrying short hairpin RNA targeting\n                    <jats:italic>Sema3e<\/jats:italic>\n                    promoted disoriented pathological neovascularization and partially abolished the inhibitory vascular effects of ROR\u03b1 deficiency in retinopathy. Our findings suggest that ROR\u03b1 is a novel transcriptional regulator of SEMA3E\u2010mediated neurovascular coupling in pathological retinal angiogenesis.\u2014Sun, Y., Liu, C.\u2010H., Wang, Z., Meng, S. S., Burnim, S. B., SanGiovanni, J. P., Kamenecka, T. M., Solt, L. A., Chen, J. ROR\u03b1 modulates semaphorin 3E transcription and neurovascular interaction in pathological retinal angiogenesis. FASEB J. 31, 4492\u20134502 (2017).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201700172r","type":"journal-article","created":{"date-parts":[[2017,6,23]],"date-time":"2017-06-23T21:00:50Z","timestamp":1498251650000},"page":"4492-4502","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["ROR\u03b1 modulates semaphorin 3E transcription and neurovascular interaction in pathological retinal angiogenesis"],"prefix":"10.1096","volume":"31","author":[{"given":"Ye","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Ophthalmology Harvard Medical School, Boston Children's Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chi\u2010Hsiu","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Harvard Medical School, Boston Children's Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongxiao","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Harvard Medical School, Boston Children's Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven S.","family":"Meng","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Harvard Medical School, Boston Children's Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuel B.","family":"Burnim","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Harvard Medical School, Boston Children's Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John Paul","family":"SanGiovanni","sequence":"additional","affiliation":[{"name":"Section of Nutritional Neuroscience National Institute on Alcohol Abuse and Alcoholism National Institutes of Health Bethesda Maryland USA"},{"name":"Department of Biochemistry and Molecular and Cellular Biology Georgetown School of Medicine Washington, D.C. USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theodore M.","family":"Kamenecka","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine The Scripps Research Institute Jupiter Florida USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura A.","family":"Solt","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology The Scripps Research Institute Jupiter Florida USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Harvard Medical School, Boston Children's Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,9,19]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1005073"},{"key":"e_1_2_8_3_1","first-page":"1162","article-title":"Mechanisms and management of retinopathy of prematurity","volume":"368","author":"Hartnett M. 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