{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:12:48Z","timestamp":1787015568915,"version":"build-2736575974"},"reference-count":31,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2015,11,27]],"date-time":"2015-11-27T00:00:00Z","timestamp":1448582400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21NS085660"],"award-info":[{"award-number":["R21NS085660"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2016,2]]},"abstract":"Abstract<\/jats:title>\n \n \n \n Inflammation is a major contributor to neuronal injury and is associated with poor outcome after acute brain injury such as stroke. The pro\u2010inflammatory cytokine interleukin (\n IL<\/jats:styled-content>\n )\u20101 is a critical regulator of cerebrovascular inflammation after ischemic injury, mainly through action of both of its isoforms,\n IL<\/jats:styled-content>\n \u20101\u03b1 and\n IL<\/jats:styled-content>\n \u20101\u03b2, at the brain endothelium. In contrast, the differential action of these ligands on endothelial activation and post\u2010stroke angiogenesis is largely unknown. Here, we demonstrate that\n IL<\/jats:styled-content>\n \u20101\u03b1 is chronically elevated in the brain after experimental stroke suggesting that it is present during post\u2010stroke angiogenic periods. Furthermore, we demonstrate that\n IL<\/jats:styled-content>\n \u20101\u03b1 is a potent mediator of endothelial activation and inducer of angiogenic markers in endothelial cells\n in\u00a0vitro<\/jats:italic>\n . Using brain endothelial cell lines, we found that\n IL<\/jats:styled-content>\n \u20101\u03b1 was significantly more potent than\n IL<\/jats:styled-content>\n \u20101\u03b2 at inducing endothelial cell activation, as measured by expression of the pro\u2010angiogenic chemokine\n CXCL<\/jats:styled-content>\n \u20101.\n IL<\/jats:styled-content>\n \u20101\u03b1 also induced strong expression of the angiogenic mediator\n IL<\/jats:styled-content>\n \u20106 in a concentration\u2010dependent manner. Furthermore,\n IL<\/jats:styled-content>\n \u20101\u03b1 induced significant proliferation and migration of endothelial cells, and promoted formation of tube\u2010like structures that are established key hallmarks of angiogenesis\n in\u00a0vitro<\/jats:italic>\n . Finally, all of those responses were blocked by the\n IL<\/jats:styled-content>\n \u20101 receptor antagonist (\n IL<\/jats:styled-content>\n \u20101\n RA<\/jats:styled-content>\n ). In conclusion, our data highlights a potential new role for\n IL<\/jats:styled-content>\n \u20101 in brain repair mechanisms and identifies\n IL<\/jats:styled-content>\n \u20101\u03b1 as a potential new therapy to promote post\u2010stroke angiogenesis.\n <\/jats:p>\n <\/jats:sec>\n \n \n \n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n Inflammation is a major contributor to neuronal injury and is associated with poor outcome after neurotrauma. We demonstrate that cytokine IL\u20101\u03b1 is chronically elevated in the brain after experimental stroke suggesting that it is present chronically post\u2010stroke. We demonstrate that IL\u20101\u03b1 is a potent mediator of endothelial activation and inducer of angiogenic markers in endothelial cells. Our data highlights a new role for IL\u20101 in brain repair mechanisms and identifies IL\u20101\u03b1 as a potential therapy to promote post\u2010stroke angiogenesis.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/jnc.13422","type":"journal-article","created":{"date-parts":[[2015,11,7]],"date-time":"2015-11-07T02:22:23Z","timestamp":1446862943000},"page":"573-580","source":"Crossref","is-referenced-by-count":53,"title":["IL<\/scp>\n \u20101alpha induces angiogenesis in brain endothelial cells\n in\u00a0vitro<\/i>\n : implications for brain angiogenesis after acute injury"],"prefix":"10.1111","volume":"136","author":[{"given":"Kathleen","family":"Salmeron","sequence":"first","affiliation":[{"name":"Sanders Brown Center on Aging University of Kentucky Lexington Kentucky USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takuma","family":"Aihara","sequence":"additional","affiliation":[{"name":"Faculty of Life Sciences University of Manchester Manchester UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Redondo\u2010Castro","sequence":"additional","affiliation":[{"name":"Faculty of Life Sciences University of Manchester Manchester UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuel","family":"Pinteaux","sequence":"additional","affiliation":[{"name":"Faculty of Life Sciences University of Manchester Manchester UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory","family":"Bix","sequence":"additional","affiliation":[{"name":"Sanders Brown Center on Aging University of Kentucky Lexington Kentucky USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,11,27]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1200409"},{"key":"e_1_2_7_3_1","doi-asserted-by":"crossref","first-page":"665","DOI":"10.1016\/S0022-3565(24)35153-5","article-title":"Characterization of interleukin\u20101a binding to mouse brain endothelial cells","volume":"291","author":"Banks W. 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