{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T22:36:00Z","timestamp":1767911760834,"version":"3.49.0"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[1998,4,20]]},"abstract":"<jats:p><jats:italic>Abstract<\/jats:italic>\u2014During the first few hours after heart transplantation, the occurrence of graft failure is unpredictable and devastating. An explosive cascade of inflammatory events within the reperfused graft vasculature is likely to be mediated, at least in part, by the local expression of the leukocyte adhesion receptor intercellular adhesion molecule-1 (ICAM-1, CD54). Furthermore, although proinflammatory cytokines such as interleukin-1 (IL-1) are known to autoinduce their own (and ICAM-1) expression in vitro, there are no data to identify their functional in vivo cross talk in the setting of isograft transplantation. To determine the role of ICAM-1 in primary graft failure, we used an isogeneic vascularized model of heterotopic cardiac transplantation. ICAM-1 mRNA and protein increased in grafts during the early posttransplant period and were predominantly localized in the endothelium. The functional significance of this was established using donor hearts obtained from either ICAM-1\u2013deficient (ICAM-1 \u2212\/\u2212) or control (ICAM-1 +\/+) mice. ICAM-1 +\/+ grafts exhibited increased neutrophil infiltration, reduced left ventricular compliance, and poorer survival than did ICAM-1 \u2212\/\u2212 grafts. Increased ICAM-1 expression was not limited to ICAM-1 +\/+ grafts but also occurred in unmanipulated recipient organs located remote from the site of surgery (but only after transplantation of ICAM-1 +\/+, not ICAM-1 \u2212\/\u2212, cardiac grafts). This expression of ICAM-1 in remote organs appeared to be triggered by IL-1\u03b1 released from the graft, because (1) in situ hybridization revealed increased IL-1 mRNA within cells of the reperfused graft, including myocytes and endothelial cells; (2) ICAM-1 expression in remote organs coincided with a significant increase in serum levels of IL-1\u03b1 after transplantation of ICAM-1 +\/+ grafts; both remote organ ICAM-1 expression and IL-1\u03b1 levels were blunted by implantation of ICAM-1 \u2212\/\u2212 grafts; and (3) remote organ ICAM-1 expression and neutrophil infiltration and IL-1 levels could be blocked by the administration of an IL-1 receptor antagonist. These data demonstrate an apparent positive-feedback loop in which local ICAM-1 and IL-1 expression leads to a mutual amplification of each other\u2019s expression within the reperfused graft, promulgating inflammatory events that are likely to be an important cause of primary cardiac graft failure. Because IL-1 receptor blockade reduces the IL-1\u2013mediated autoinduction of IL-1, reduces the expression of ICAM-1 in both the graft and remote organs, and improves graft survival, it may provide a new and effective strategy to prevent the occurrence of primary cardiac graft failure.<\/jats:p>","DOI":"10.1161\/01.res.82.7.762","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:47:05Z","timestamp":1339462025000},"page":"762-772","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":39,"title":["Cardiac Graft Intercellular Adhesion Molecule-1 (ICAM-1) and Interleukin-1 Expression Mediate Primary Isograft Failure and Induction of ICAM-1 in Organs Remote From the Site of Transplantation"],"prefix":"10.1161","volume":"82","author":[{"given":"Catherine Y.","family":"Wang","sequence":"first","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshifumi","family":"Naka","sequence":"additional","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Liao","sequence":"additional","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mehmet C.","family":"Oz","sequence":"additional","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy A.","family":"Springer","sequence":"additional","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jose-Carlos","family":"Gutierrez-Ramos","sequence":"additional","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David J.","family":"Pinsky","sequence":"additional","affiliation":[{"name":"From Columbia University (C.Y.W., Y.N., H.L., M.C.O., D.J.P.), College of Physicians and Surgeons, New York, NY, and The Center for Blood Research (T.A.S., J.-C.G.-R.), Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"353","volume":"13","year":"1994","unstructured":"Young JB, Naftel DC, Bourge RC, Kirklin JK, Clemson BS, Porter CB, Rpdeheffer RJ, Kenzora JL. 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