{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T22:40:09Z","timestamp":1792708809416,"version":"4.5.0"},"reference-count":41,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2014,4,30]],"date-time":"2014-04-30T00:00:00Z","timestamp":1398816000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:p>Lipocalin-2 (LCN2) is a secreted protein of the lipocalin family, but little is known about the expression or the role of LCN2 in the central nervous system. Here, we investigated the role of LCN2 in ischemic stroke using a rodent model of transient cerebral ischemia. Lipocalin-2 expression was highly induced in the ischemic brain and peaked at 24 hours after reperfusion. After transient middle cerebral artery occlusion, LCN2 was predominantly expressed in astrocytes and endothelial cells, whereas its receptor (24p3R) was mainly detected in neurons, astrocytes, and endothelial cells. Brain infarct volumes, neurologic scores, blood\u2013brain barrier (BBB) permeabilities, glial activation, and inflammatory mediator expression were significantly lower in LCN2-defkient mice than in wild-type animals. Lipocalin-2 deficiency also attenuated glial neurotoxicity in astrocyte\/neuron cocultures after oxygen-glucose deprivation. Our results indicate LCN2 has a critical role in brain injury after ischemia\/reperfusion, and that LCN2 may contribute to neuronal cell death in the ischemic brain by promoting neurotoxic glial activation, neuroinflammation, and BBB disruption.<\/jats:p>","DOI":"10.1038\/jcbfm.2014.83","type":"journal-article","created":{"date-parts":[[2014,4,30]],"date-time":"2014-04-30T04:00:58Z","timestamp":1398830458000},"page":"1306-1314","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":150,"title":["Lipocalin-2 Deficiency Attenuates Neuroinflammation and Brain Injury after Transient Middle Cerebral Artery Occlusion in Mice"],"prefix":"10.1177","volume":"34","author":[{"given":"Myungwon","family":"Jin","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, Daegu, Republic of Korea"},{"name":"Department of Biomedical Sciences, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jong-Heon","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, Daegu, Republic of Korea"},{"name":"Department of Biomedical Sciences, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eunha","family":"Jang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Brain Science & Engineering Institute, Kyungpook National University School of Medicine, Daegu, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young 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