{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T17:03:56Z","timestamp":1788282236999,"version":"build-2803163510"},"reference-count":33,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2015,10,16]],"date-time":"2015-10-16T00:00:00Z","timestamp":1444953600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","award":["MOP 102535"],"award-info":[{"award-number":["MOP 102535"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Multiple mechanisms contribute to progressive cardiac dysfunction after myocardial infarction (<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>) and inflammation is an important mediator. Mast cells (<jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s) trigger inflammation after <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> by releasing bio\u2010active factors that contribute to healing. c\u2010Kit\u2010deficient (<jats:italic>Kit<\/jats:italic><jats:sup><jats:italic>W\/W\u2010v<\/jats:italic><\/jats:sup>) mice have dysfunctional <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s and develop severe ventricular dilatation post\u2010<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. We explored the role of <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s in post\u2010<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> repair. Mouse wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) and <jats:italic>Kit<\/jats:italic><jats:sup><jats:italic>W\/W\u2010v<\/jats:italic><\/jats:sup> <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s were obtained from bone marrow (<jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content>). <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> effects on fibroblasts were examined <jats:italic>in vitro<\/jats:italic> by proliferation and gel contraction assays. <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s were implanted into infarcted mouse hearts and their effects were evaluated using molecular, cellular and cardiac functional analyses. In contrast to <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>,<jats:italic> Kit<\/jats:italic><jats:sup><jats:italic>W\/W\u2010v<\/jats:italic><\/jats:sup> <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> transplantation into <jats:italic>Kit<\/jats:italic><jats:sup><jats:italic>W\/W\u2010v<\/jats:italic><\/jats:sup> mice did not improve cardiac function or scar size post\u2010<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. <jats:italic>Kit<\/jats:italic><jats:sup><jats:italic>W\/W\u2010v<\/jats:italic><\/jats:sup> <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s induced significantly reduced fibroblast proliferation and contraction compared to <jats:styled-content style=\"fixed-case\">WT MC<\/jats:styled-content>s. <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> influence on fibroblast proliferation was Basic fibroblast growth factor (bFGF)\u2010dependent and <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>\u2010induced fibroblast contractility functioned through transforming growth factor (<jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>)\u2010\u03b2. <jats:styled-content style=\"fixed-case\">WT MC<\/jats:styled-content>s transiently rescue cardiac function early post\u2010<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>, but the benefits of <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content> cell implantation lasted longer. <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s induced increased inflammation compared to the <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content>\u2010injected mice, with increased neutrophil infiltration and infarct tumour necrosis factor\u2010\u03b1 (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1) concentration. This augmented inflammation was followed by increased angiogenesis and myofibroblast formation and reduced scar size at early time\u2010points. Similar to the functional data, these beneficial effects were transient, largely vanishing by day 28. Dysfunctional <jats:italic>Kit<\/jats:italic><jats:sup><jats:italic>W\/W\u2010v<\/jats:italic><\/jats:sup> <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s were unable to rescue cardiac function post\u2010<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">WT MC<\/jats:styled-content> implantation transiently enhanced angiogenesis and cardiac function. These data suggest that increased inflammation is beneficial to cardiac repair, but these effects are not persistent.<\/jats:p>","DOI":"10.1111\/jcmm.12703","type":"journal-article","created":{"date-parts":[[2015,10,16]],"date-time":"2015-10-16T07:52:47Z","timestamp":1444981967000},"page":"2751-2762","source":"Crossref","is-referenced-by-count":16,"title":["The cardiac repair benefits of inflammation do not persist: evidence from mast cell implantation"],"prefix":"10.1111","volume":"19","author":[{"given":"Zhengbo","family":"Shao","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Surgery Toronto General Research Institute University Health Network Toronto ON Canada"},{"name":"Division of Cardiac Surgery Department of Surgery University of Toronto Toronto ON Canada"},{"name":"Department of Ophthalmology Second Affiliated Hospital of Harbin Medical University Harbin 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