{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T14:53:22Z","timestamp":1782831202771,"version":"3.54.5"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,11,7]],"date-time":"2014-11-07T00:00:00Z","timestamp":1415318400000},"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":["R21 NS 070003"],"award-info":[{"award-number":["R21 NS 070003"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Emmerling Foundation"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuropathology"],"published-print":{"date-parts":[[2015,4]]},"abstract":"Traumatic brain injury (TBI<\/jats:styled-content>) is accompanied by inflammatory infiltrates and CNS<\/jats:styled-content> tissue response. The astrocytosis associated with TBI<\/jats:styled-content> has been proposed to have both beneficial and detrimental effects on surviving neural tissue. We recently observed prominent astrocytic expression of YKL<\/jats:styled-content>\u201040\/chitinase 3\u2010like protein 1 (CHI3L1<\/jats:styled-content>) associated with severity of brain injury. The physiological role of CHI3L1<\/jats:styled-content> in the CNS<\/jats:styled-content> is unknown; however, its distribution at the perimeter of contusions and temporal course of expression suggested that in TBI<\/jats:styled-content> it might be an important component of the astrocytic response to modulate CNS<\/jats:styled-content> inflammation. To address this hypothesis, we used serially sectioned brains to quantitatively compare the neuropathological outcomes of TBI produced by controlled cortical impact in wild type (WT<\/jats:styled-content>) and chi3l1<\/jats:italic> knockout (KO<\/jats:styled-content>) mice where the murine YKL<\/jats:styled-content>\u201040 homologue, breast regression protein 39 (BRP<\/jats:styled-content>\u201039\/CHI3l1<\/jats:styled-content>)<\/jats:italic>, had been homozygously disrupted. At 21 days post\u2010injury, chi3l1<\/jats:italic>\u2005KO<\/jats:styled-content> mice displayed greater astrocytosis (increased GFAP<\/jats:styled-content> staining) in the hemispheres ipsilateral and contralateral to impact compared with WT<\/jats:styled-content> mice. Similarly, Iba1 expression as a measure of microglial\/macrophage response was significantly increased in chi3l1<\/jats:italic>\u2005KO<\/jats:styled-content> compared with WT<\/jats:styled-content> in the hemisphere contralateral to impact. We conclude that astrocytic expression of CHI3L1<\/jats:styled-content> limits the extent of both astrocytic and microglial\/macrophage facets of neuroinflammation and suggests a novel potential therapeutic target for modulating neuroinflammation.<\/jats:p>","DOI":"10.1111\/neup.12158","type":"journal-article","created":{"date-parts":[[2014,11,7]],"date-time":"2014-11-07T08:04:49Z","timestamp":1415347489000},"page":"95-106","source":"Crossref","is-referenced-by-count":41,"title":["Role for mammalian chitinase 3\u2010like protein 1 in traumatic brain injury"],"prefix":"10.1111","volume":"35","author":[{"given":"Clayton A.","family":"Wiley","sequence":"first","affiliation":[{"name":"Department of Pathology University of Pittsburgh Pittsburgh Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dafna","family":"Bonneh\u2010Barkay","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Pittsburgh Pittsburgh Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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