{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T15:58:22Z","timestamp":1774972702978,"version":"3.50.1"},"reference-count":28,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2009,12,8]],"date-time":"2009-12-08T00:00:00Z","timestamp":1260230400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2010,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Secondary neurodegeneration resulting from stroke is mediated by delayed proinflammatory signaling and immune cell activation. Although it remains unknown which cell surface markers signify a proinflammatory phenotype, increased isolectin binding occurs on CD11b\u2010expressing immune cells within injured brain tissue. Several reports have confirmed the efficacy of human umbilical cord blood (HUCB) cell therapy in reducing ischemic injury in rat after middle cerebral artery occlusion (MCAO), and these effects were attributed in part to dampened neuroinflammation. The present study examined the time course of lectin binding to cells of microglia\/macrophage lineage within 96 hr after MCAO and whether delayed HUCB cell treatment alters the migration and\/or morphological characteristics of these cells throughout the period of infarct expansion. Isolectin binding was up\u2010regulated in response to injury, was maximal at 96 hr, and colocalized with cells that expressed the putative proinflammatory markers MMP\u20109 and nitric oxide. Isolectin\u2010tagged fluorescence was also significantly increased at 72 hr and localized to greater numbers of amoeboid, CD11b\u2010expressing cells relative to 51 hr. Treatment with 1 \u00d7 10<jats:sup>6<\/jats:sup> HUCB cells significantly reduced total lectin binding at 72 hr, as well as the total area occupied by lectin\u2010tagged fluorescence at both 51 and 72 hr, relative to vehicle\u2010treated controls. This effect was accompanied by a shift in the morphology of CD11b\u2010positive cells from amoeboid to ramified shape. These data indicate that HUCB cell therapy suppressed the recruitment of proinflammatory, isolectin\u2010binding cells during the period of infarct expansion, thus offering a potential mechanism for the protective effects of HUCB cell therapy. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22306","type":"journal-article","created":{"date-parts":[[2009,12,8]],"date-time":"2009-12-08T22:13:36Z","timestamp":1260310416000},"page":"1213-1222","source":"Crossref","is-referenced-by-count":38,"title":["Human umbilical cord blood cell therapy blocks the morphological change and recruitment of CD11b\u2010expressing, isolectin\u2010binding proinflammatory cells after middle cerebral artery occlusion"],"prefix":"10.1002","volume":"88","author":[{"given":"Christopher C.","family":"Leonardo","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aaron 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