{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T07:16:42Z","timestamp":1775200602364,"version":"3.50.1"},"reference-count":39,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,4,22]],"date-time":"2017-04-22T00:00:00Z","timestamp":1492819200000},"content-version":"vor","delay-in-days":21,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"publisher","award":["SCHI 1330\/1\u20101"],"award-info":[{"award-number":["SCHI 1330\/1\u20101"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000011","name":"Howard Hughes Medical Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000011","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["NS040511"],"award-info":[{"award-number":["NS040511"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["P01NS083513"],"award-info":[{"award-number":["P01NS083513"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HD052064"],"award-info":[{"award-number":["R01 HD052064"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Neonatal white matter injury (NWMI) is a lesion found in preterm infants that can lead to cerebral palsy. Although antagonists of bone morphogenetic protein (BMP) signaling, such as Noggin, promote oligodendrocyte precursor cell (OPC) production after hypoxic\u2010ischemic (HI) injury, the downstream functional targets are poorly understood. The basic helix\u2010loop\u2010helix protein, oligodendrocyte transcription factor 1 (Olig1), promotes oligodendrocyte (OL) development and is essential during remyelination in adult mice. Here, we investigated whether <jats:italic>Olig1<\/jats:italic> function is required downstream of BMP antagonism for response to injury in the neonatal brain.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used wild\u2010type and <jats:italic>Olig1<\/jats:italic>\u2010null mice subjected to neonatal stroke and postnatal neural progenitor cultures, and we analyzed Olig1 expression in human postmortem samples from neonates that suffered HI encephalopathy (HIE).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Olig1<\/jats:italic>\u2010null neonatal mice showed significant hypomyelination after moderate neonatal stroke. Surprisingly, damaged white matter tracts in <jats:italic>Olig1<\/jats:italic>\u2010null mice lacked Olig2<jats:sup>+<\/jats:sup> OPCs, and instead proliferating neuronal precursors and GABAergic interneurons were present. We demonstrate that Noggin\u2010induced OPC production requires <jats:italic>Olig1<\/jats:italic> function. In postnatal neural progenitors, Noggin governs production of OLs versus interneurons through <jats:italic>Olig1<\/jats:italic>\u2010mediated repression of <jats:italic>Dlx1\/2<\/jats:italic> transcription factors. Additionally, we observed that Olig1 and the BMP signaling effector, phosphorylated SMADs (Sma\u2010 and Mad\u2010related proteins) 1, 5, and 8, were elevated in the subventricular zone of human infants with HIE compared to controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>These findings indicate that <jats:italic>Olig1<\/jats:italic> has a critical function in regulation of postnatal neural progenitor cell production in response to Noggin. Ann Neurol 2017;81:560\u2013571<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.24907","type":"journal-article","created":{"date-parts":[[2017,3,2]],"date-time":"2017-03-02T23:16:44Z","timestamp":1488496604000},"page":"560-571","source":"Crossref","is-referenced-by-count":15,"title":["<i>Olig1<\/i> is required for noggin\u2010induced neonatal myelin repair"],"prefix":"10.1002","volume":"81","author":[{"given":"Jennifer K.","family":"Sabo","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Eli and Edythe Broad Center for Stem Cell Research and Regeneration Medicine University of California San Francisco, San Francisco CA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vivi","family":"Heine","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Eli and Edythe Broad Center for Stem Cell Research and Regeneration Medicine University of California San Francisco, San Francisco 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