{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T10:50:58Z","timestamp":1790247058037,"version":"4.1.0"},"reference-count":63,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T00:00:00Z","timestamp":1571356800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","award":["BB\/J018635\/1"],"award-info":[{"award-number":["BB\/J018635\/1"]}],"id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Glia"],"published-print":{"date-parts":[[2020,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Postnatal subventricular zone (SVZ) neural stem cells generate forebrain glia, namely astrocytes and oligodendrocytes. The cues necessary for this process are unclear, despite this phase of brain development being pivotal in forebrain gliogenesis. Galectin\u20103 (Gal\u20103) is increased in multiple brain pathologies and thereby regulates astrocyte proliferation and inflammation in injury. To study the function of Gal\u20103 in inflammation and gliogenesis, we carried out functional studies in mouse. We overexpressed Gal\u20103 with electroporation and using immunohistochemistry surprisingly found no inflammation in the healthy postnatal SVZ. This allowed investigation of inflammation\u2010independent effects of Gal\u20103 on gliogenesis. Loss of Gal\u20103 function via knockdown or conditional knockout reduced gliogenesis, whereas Gal\u20103 overexpression increased it. Gal\u20103 overexpression also increased the percentage of striatal astrocytes generated by the SVZ but decreased the percentage of oligodendrocytes. These novel findings were further elaborated with multiple analyses demonstrating that Gal\u20103 binds to the bone morphogenetic protein receptor one alpha (BMPR1\u03b1) and increases bone morphogenetic protein (BMP) signaling. Conditional knockout of BMPR1\u03b1 abolished the effect of Gal\u20103 overexpression on gliogenesis. Gain\u2010of\u2010function of Gal\u20103 is relevant in pathological conditions involving the human forebrain, which is particularly vulnerable to hypoxia\/ischemia during perinatal gliogenesis. Hypoxic\/ischemic injury induces astrogliosis, inflammation and cell death. We show that Gal\u20103 immunoreactivity was increased in the perinatal human SVZ and striatum after hypoxia\/ischemia. Our findings thus show a novel inflammation\u2010independent function for Gal\u20103; it is necessary for gliogenesis and when increased in expression can induce astrogenesis via BMP signaling.<\/jats:p>","DOI":"10.1002\/glia.23730","type":"journal-article","created":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T15:41:41Z","timestamp":1571413301000},"page":"435-450","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Galectin\u20103 modulates postnatal subventricular zone gliogenesis"],"prefix":"10.1002","volume":"68","author":[{"given":"Osama","family":"Al\u2010Dalahmah","sequence":"first","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"},{"name":"Department of Pathology and Cell Biology Columbia University Medical Center  New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luana","family":"Campos Soares","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"},{"name":"Department of Oncology University of Oxford  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Nicholson","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Swip","family":"Draijer","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mayara","family":"Mundim","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victor 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