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There is growing evidence indicating the involvement of\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015 in various pathologies. Expression of\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015 is induced under conditions of inflammation and increased\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015 serum levels are suggested as a risk factor for cardiovascular diseases.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              We show here that\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015 and proinflammatory cytokine interleukin (\n              <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n              )\u20106 levels are highly increased (5\u2010fold) in cultured oxidized low\u2010density lipoproteins\u2013stimulated peritoneal macrophages derived from\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015\n              <jats:sup>+\/+<\/jats:sup>\n              \/apolipoprotein (apo)\n              <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              , mice. Notably,\n              <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n              \u20106 induction on oxidized low\u2010density lipoproteins stimulation is completely abolished in the absence of\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015. Consistent with our in vitro data\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015\n              <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n              expression and protein levels are upregulated (2.5\u2010 to 6\u2010fold) in the atherosclerotic vessel wall of\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015\n              <jats:sup>+\/+<\/jats:sup>\n              \/apo\n              <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice after a cholesterol\u2010enriched diet.\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015 deficiency inhibits lumen stenosis (52%) and\n              <jats:sup>18<\/jats:sup>\n              <jats:styled-content style=\"fixed-case\">FDG<\/jats:styled-content>\n              uptake (34%) in the aortic arch despite increased serum triglyceride\/cholesterol levels and elevated body weight. Immunohistomorphometric investigations of atherosclerotic lesions reveal a decreased percentage of inflammatory\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              11b\n              <jats:sup>+<\/jats:sup>\n              (57%) or\n              <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n              \u20106\n              <jats:sup>+<\/jats:sup>\n              , leukocytes, and apoptotic cells (74%) after 20\u00a0weeks. However, the total number of macrophages and cell density in atherosclerotic lesions of the innominate artery are increased in\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              \/apo\n              <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Our data suggest that\n              <jats:styled-content style=\"fixed-case\">GDF<\/jats:styled-content>\n              \u201015 is involved in orchestrating atherosclerotic lesion progression by regulating apoptotic cell death and\n              <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n              \u20106\u2013dependent inflammatory responses to vascular injury.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.112.002550","type":"journal-article","created":{"date-parts":[[2013,5,24]],"date-time":"2013-05-24T16:46:09Z","timestamp":1369413969000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":160,"title":["Growth Differentiation Factor\u201015 Deficiency Inhibits Atherosclerosis Progression by Regulating Interleukin\u20106\u2013Dependent Inflammatory Response to Vascular Injury"],"prefix":"10.1161","volume":"1","author":[{"given":"Gabriel A.","family":"Bonaterra","sequence":"first","affiliation":[{"name":"Institute of Anatomy and Cell Biology, Department of Medical Cell Biology, University of Marburg, Marburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefanie","family":"Z\u00fcgel","sequence":"additional","affiliation":[{"name":"Institute of Anatomy and Cell Biology, Department of Medical Cell Biology, University of Marburg, Marburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel","family":"Thogersen","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabrina A.","family":"Walter","sequence":"additional","affiliation":[{"name":"Institute of Anatomy and Cell Biology, Department of Medical Cell Biology, University of Marburg, Marburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uwe","family":"Haberkorn","sequence":"additional","affiliation":[{"name":"Department of Nuclear Medicine, University Hospital of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens","family":"Strelau","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralf","family":"Kinscherf","sequence":"additional","affiliation":[{"name":"Institute of Anatomy and Cell Biology, Department of Medical Cell Biology, University of Marburg, Marburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2010.06.010"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.21.11514"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004410051337"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.65.1.2"},{"key":"e_1_3_4_6_2","first-page":"273","article-title":"GDF\u201015\/MIC\u20101 a novel member of the TGF\u2010beta superfamily","volume":"60","author":"Strelau J","year":"2000","unstructured":"Strelau J, Bottner M, Lingor P, Suter\u2010Crazzolara C, Galter D, Jaszai J, Sullivan A, Schober A, Krieglstein K, Unsicker K. 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