{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T09:56:14Z","timestamp":1790762174081,"version":"4.1.0"},"reference-count":58,"publisher":"National Academy of Sciences","issue":"17","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1998,8,18]]},"abstract":"<jats:p>\n                    Leukocytes are recruited early and abundantly to experimentally injured vessels, in direct proportion to cell proliferation and intimal growth. Activated circulating leukocytes and Mac-1 (CD11b\/CD18, \u03b1\n                    <jats:sub>M<\/jats:sub>\n                    \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    ) expression are markers of restenosis risk in patients undergoing angioplasty. As angioplastied vessels lack endothelium but have extensive fibrin(ogen) and platelet deposition, we hypothesized that Mac-1-dependent adhesion to fibrin(ogen) is an important determinant of leukocyte recruitment and function, which may in turn promote intimal growth. To study this hypothesis we administered M1\/70, an anti-CD11b blocking mAb, to rabbits (1 mg\/kg i.v.) immediately before, and every 48 hr for 3, 6, or 14 days after, iliac artery balloon denudation or deeper stent-induced injury. M1\/70, which bound to isolated rabbit monocytes and dose-dependently inhibited Mac-1-mediated fibrinogen binding\n                    <jats:italic>in vitro<\/jats:italic>\n                    , reduced leukocyte recruitment more than 2-fold 3, 6, and 14 days after injury. Neointimal growth 14 days after injury was markedly attenuated by treatment with M1\/70 (intimal area after balloon injury, 0.12 \u00b1 0.09 mm\n                    <jats:sup>2<\/jats:sup>\n                    , compared with 0.32 \u00b1 0.08 mm\n                    <jats:sup>2<\/jats:sup>\n                    in vehicle-treated controls,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01, and 0.38 \u00b1 0.08 mm\n                    <jats:sup>2<\/jats:sup>\n                    in IgG-treated controls,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.005; intimal area after stent injury, 0.56 \u00b1 0.16 mm\n                    <jats:sup>2<\/jats:sup>\n                    , compared with 0.84 \u00b1 0.13 mm\n                    <jats:sup>2<\/jats:sup>\n                    in vehicle-treated controls,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05, and 0.90 \u00b1 0.15 mm\n                    <jats:sup>2<\/jats:sup>\n                    in IgG-treated controls,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.02). Mac-1 blockade reduces experimental neointimal thickening, suggesting that leukocyte recruitment to and infiltration of injured arteries may be a valid target for preventing intimal hyperplasia.\n                  <\/jats:p>","DOI":"10.1073\/pnas.95.17.10134","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:39:15Z","timestamp":1027679955000},"page":"10134-10139","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":201,"title":["A mAb to the \u03b2\n                    <sub>2<\/sub>\n                    -leukocyte integrin Mac-1 (CD11b\/CD18) reduces intimal thickening after angioplasty or stent implantation in rabbits"],"prefix":"10.1073","volume":"95","author":[{"given":"Campbell","family":"Rogers","sequence":"first","affiliation":[{"name":"Department of Medicine, Cardiac Catheterization Laboratory and Coronary Care Unit, Cardiovascular Division, Brigham and Women\u2019s Hospital, Harvard 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