{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T14:20:07Z","timestamp":1791037207941,"version":"4.1.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Objective\u2014<\/jats:italic>\n            <\/jats:bold>\n            To determine the role of monocyte chemoattractant protein-1 (Mcp-1) on the progression of visceral fat-induced atherosclerosis.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            Visceral fat inflammation was induced by transplantation of perigonadal fat. To determine whether recipient Mcp-1 status affected atherosclerosis induced by inflammatory fat, apolipoprotein E-deficient (\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) and\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            and Mcp-1-deficient (\n            <jats:italic>Mcp-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) mice underwent visceral fat transplantation. Intravital microscopy was used to study leukocyte-endothelial interactions. To study the primary tissue source of circulating Mcp-1, both fat and bone marrow transplantation experiments were used. Transplantation of visceral fat increased atherosclerosis in\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice but had no effect on atherosclerosis in\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ,\n            <jats:italic>Mcp-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Intravital microscopy revealed increased leukocyte attachment to the endothelium in\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice compared with\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ,\n            <jats:italic>Mcp-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice after receiving visceral fat transplants. Transplantation of visceral fat increased plasma Mcp-1, although donor adipocytes were not the source of circulating Mcp-1 because no Mcp-1 was detected in plasma from\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ,\n            <jats:italic>Mcp-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice transplanted with\n            <jats:italic>Wt<\/jats:italic>\n            fat, indicating that recipient Mcp-1-producing cells were affecting the atherogenic response to the fat transplantation. Consistently, transplantation of\n            <jats:italic>Mcp-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            fat to\n            <jats:italic>ApoE<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice did not lead to atheroprotection in recipient mice. Bone marrow transplantation between\n            <jats:italic>Wt<\/jats:italic>\n            and\n            <jats:italic>Mcp-1<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice indicated that the primary tissue source of circulating Mcp-1 was the endothelium.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusion\u2014<\/jats:italic>\n            <\/jats:bold>\n            Recipient Mcp-1 deficiency protects against atherosclerosis induced by transplanted visceral adipose tissue.\n          <\/jats:p>","DOI":"10.1161\/atvbaha.110.205914","type":"journal-article","created":{"date-parts":[[2010,3,19]],"date-time":"2010-03-19T02:25:33Z","timestamp":1268965533000},"page":"1151-1158","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":46,"title":["Monocyte Chemoattractant Protein-1 Deficiency Protects Against Visceral Fat-Induced Atherosclerosis"],"prefix":"10.1161","volume":"30","author":[{"given":"Miina K.","family":"O\u0308hman","sequence":"first","affiliation":[{"name":"From Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew P.","family":"Wright","sequence":"additional","affiliation":[{"name":"From Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin J.","family":"Wickenheiser","sequence":"additional","affiliation":[{"name":"From Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Luo","sequence":"additional","affiliation":[{"name":"From Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hana M.","family":"Russo","sequence":"additional","affiliation":[{"name":"From Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel T.","family":"Eitzman","sequence":"additional","affiliation":[{"name":"From Cardiovascular Research Center, Department of Internal Medicine, University of Michigan, Ann Arbor, 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