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A specialized cell-cell adhesion protein, cadherin-11 (CDH11), contributes to inflammation and fibrosis in rheumatoid arthritis, pulmonary fibrosis, and aortic valve calcification but has not been studied in myocardium after MI. MI was induced by ligation of the left anterior descending artery in mice with either heterozygous or homozygous knockout of CDH11, wild-type mice receiving bone marrow transplants from\n                    <jats:italic>Cdh11<\/jats:italic>\n                    -deficient animals, and wild-type mice treated with a functional blocking antibody against CDH11 (SYN0012). Flow cytometry revealed significant CDH11 expression in noncardiomyocyte cells after MI. Animals given SYN0012 had improved cardiac function, as measured by echocardiogram, reduced tissue remodeling, and altered transcription of inflammatory and proangiogenic genes. Targeting CDH11 reduced bone marrow\u2013derived myeloid cells and increased proangiogenic cells in the heart 3 days after MI. Cardiac fibroblast and macrophage interactions increased IL-6 secretion in vitro. Our findings suggest that CDH11-expressing cells contribute to inflammation-driven fibrotic remodeling after MI and that targeting CDH11 with a blocking antibody improves outcomes by altering recruitment of bone marrow\u2013derived cells, limiting the macrophage-induced expression of IL-6 by fibroblasts and promoting vascularization.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.131545","type":"journal-article","created":{"date-parts":[[2019,9,18]],"date-time":"2019-09-18T11:00:55Z","timestamp":1568804455000},"source":"Crossref","is-referenced-by-count":48,"title":["Cadherin-11 blockade reduces inflammation-driven fibrotic remodeling and improves outcomes after myocardial infarction"],"prefix":"10.1172","volume":"4","author":[{"given":"Alison K.","family":"Schroer","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew R.","family":"Bersi","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cynthia R.","family":"Clark","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinkun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lehanna H.","family":"Sanders","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonis K.","family":"Hatzopoulos","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas L.","family":"Force","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1005-1552","authenticated-orcid":true,"given":"Susan M.","family":"Majka","sequence":"additional","affiliation":[{"name":"Department of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University, Nashville, Tennessee, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8980-9874","authenticated-orcid":true,"given":"Hind","family":"Lal","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9662-1503","authenticated-orcid":true,"given":"W. 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