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Although CtsB was reported to promote and reduce angiogenesis, there is no mechanistic explanation that reconciles this apparent discrepancy. CtsB cleaves CD18 from the surface of immune cells, but its contribution to angiogenesis has not been studied. We developed an\n                    <jats:italic>in vivo<\/jats:italic>\n                    technique for visualization of immune cell transmigration from corneal vessels toward implanted cytokines. Wild\u2010type (WT) leukocytes extravasated from limbal vessels, angiogenic stalks, and growing tip vessels and migrated toward the cytokines, indicating immune competence of angiogenic vessels. Compared to WT leukocytes,\n                    <jats:italic>CtsB<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    leukocytes accumulated in a higher number in angiogenic vessels, but extravasated less toward the implanted cytokine. The accumulated\n                    <jats:italic>CtsB<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    leukocytes in angiogenic vessels expressed more CD18.\n                    <jats:italic>CD18<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    leukocytes extravasated later than WT leukocytes. However, once extravasated,\n                    <jats:italic>CD18<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    leukocytes transmigrated more rapidly than their WT counterparts. These results suggest that, although CD18 facilitates efficient extravasation, outside of the vessel CD18 interaction with the extracellular matrix, it reduced transmigration velocity. Our results reveal an unexpected role for CtsB in leukocyte extravasation and transmigration, which advances our understanding of the complex contribution of CtsB to angiogenesis.\u2014 Nakao, S., Zandi, S., Sun, D., Hafezi\u2010Moghadam, A. Cathepsin B\u2010mediated CD18 shedding regulates leukocyte recruitment from angiogenic vessels. FASEB J. 32, 143\u2010154 (2018).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201601229r","type":"journal-article","created":{"date-parts":[[2017,9,13]],"date-time":"2017-09-13T20:25:46Z","timestamp":1505334346000},"page":"143-154","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Cathepsin B\u2010mediated CD18 shedding regulates leukocyte recruitment from angiogenic vessels"],"prefix":"10.1096","volume":"32","author":[{"given":"Shintaro","family":"Nakao","sequence":"first","affiliation":[{"name":"Molecular Biomarkers Nano\u2010Imaging Laboratory Department of Radiology Brigham and Women's Hospital, Harvard Medical School Boston Massachusetts USA"},{"name":"Department of Ophthalmology Graduate School of Medical Sciences, Kyushu University Fukuoka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Souska","family":"Zandi","sequence":"additional","affiliation":[{"name":"Molecular Biomarkers Nano\u2010Imaging Laboratory Department of Radiology Brigham and Women's Hospital, Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dawei","family":"Sun","sequence":"additional","affiliation":[{"name":"Molecular Biomarkers Nano\u2010Imaging Laboratory Department of Radiology Brigham and Women's Hospital, Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ali","family":"Hafezi\u2010Moghadam","sequence":"additional","affiliation":[{"name":"Molecular Biomarkers Nano\u2010Imaging Laboratory Department of Radiology Brigham and Women's Hospital, Harvard Medical School Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,9,13]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1636908"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI23298"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0601807103"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/nri2852"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrc2353"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2010-02-267427"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.2.545"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm877"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1747.1998.00262.x"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.11-9119"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.070172"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.01.011"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.11-8114"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2013.11.010"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-7924com"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4613-0335-0_35"},{"key":"e_1_2_8_18_1","first-page":"443","article-title":"Cathepsin cysteine proteases are effectors of invasive growth and angiogenesis during multistage tumorigenesis","volume":"5","author":"Joyce J. 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