{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T16:08:05Z","timestamp":1792858085379,"version":"4.5.0"},"reference-count":56,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2019,5,10]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Immediate changes in the ECM (extracellular matrix) microenvironment occur after myocardial ischemia and reperfusion (I\/R) injury.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Aim of this study was to unravel the role of the early hyaluronan (HA)-rich ECM after I\/R.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              Genetic deletion of\n              <jats:italic>Has2<\/jats:italic>\n              and\n              <jats:italic>Has1<\/jats:italic>\n              was used in a murine model of cardiac I\/R. Chemical exchange saturation transfer imaging was adapted to image cardiac ECM post-I\/R. Of note, the cardiac chemical exchange saturation transfer signal was severely suppressed by\n              <jats:italic>Has2<\/jats:italic>\n              deletion and pharmacological inhibition of HA synthesis 24 hours after I\/R.\n              <jats:italic>Has2<\/jats:italic>\n              KO (\n              <jats:italic>Has2<\/jats:italic>\n              deficient) mice showed impaired hemodynamic function suggesting a protective role for endogenous HA synthesis. In contrast to\n              <jats:italic>Has2<\/jats:italic>\n              deficiency,\n              <jats:italic>Has1<\/jats:italic>\n              -deficient mice developed no specific phenotype compared with control post-I\/R. Importantly, in\n              <jats:italic>Has2<\/jats:italic>\n              KO mice, cardiac macrophages were diminished after I\/R as detected by\n              <jats:sup>19<\/jats:sup>\n              F MRI (magnetic resonance imaging) of perfluorcarbon-labeled immune cells, Mac-2\/Galectin-3 immunostaining, and FACS (fluorescence-activated cell sorting) analysis (CD45\n              <jats:sup>+<\/jats:sup>\n              CD11b\n              <jats:sup>+<\/jats:sup>\n              Ly6G\n              <jats:sup>\u2212<\/jats:sup>\n              CD64\n              <jats:sup>+<\/jats:sup>\n              F4\/80\n              <jats:sup>+<\/jats:sup>\n              cells). In contrast to macrophages, cardiac Ly6C\n              <jats:sup>high<\/jats:sup>\n              and Ly6C\n              <jats:sup>low<\/jats:sup>\n              monocytes were unaffected post-I\/R compared with control mice. Mechanistically, inhibition of HA synthesis led to increased macrophage apoptosis in vivo and in vitro. In addition, \u03b1-SMA (\u03b1-smooth muscle actin)\u2013positive cells were reduced in the infarcted myocardium and in the border zone. In vitro, the myofibroblast response as measured by\n              <jats:italic>Acta2<\/jats:italic>\n              mRNA expression was reduced by inhibition of HA synthesis and of CD44 signaling. Furthermore,\n              <jats:italic>Has2<\/jats:italic>\n              KO fibroblasts were less able to contract collagen gels in vitro. The effects of HA\/CD44 on fibroblasts and macrophages post-I\/R might also affect intercellular cross talk because cardiac fibroblasts were activated by monocyte\/macrophages and, in turn, protected macrophages from apoptosis.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Increased HA synthesis contributes to postinfarct healing by supporting macrophage survival and by promoting the myofibroblast response. Additionally, imaging of cardiac HA by chemical exchange saturation transfer post-I\/R might have translational value.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.118.313285","type":"journal-article","created":{"date-parts":[[2019,3,27]],"date-time":"2019-03-27T16:57:52Z","timestamp":1553705872000},"page":"1433-1447","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":72,"title":["Cardiac Hyaluronan Synthesis Is Critically Involved in the Cardiac Macrophage Response and Promotes Healing After Ischemia Reperfusion Injury"],"prefix":"10.1161","volume":"124","author":[{"given":"Anne","family":"Petz","sequence":"first","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (A.P., M.G., D.J.G., M.A., M.P., R.S., S.H., J.M., S.G., J.W.F.), University Hospital, Heinrich-Heine-University D\u00fcsseldorf, Germany"},{"name":"CARID, Cardiovascular Research Institute D\u00fcsseldorf (A.P., M.G., D.J.G., M.A., M.P., R.S., S.H., J.M., S.G., M. Kelm, A.G., U.F., J.W.F.), University Hospital, Heinrich-Heine-University D\u00fcsseldorf, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Grandoch","sequence":"additional","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (A.P., M.G., D.J.G., M.A., M.P., R.S., S.H., J.M., S.G., J.W.F.), University Hospital, Heinrich-Heine-University D\u00fcsseldorf, Germany"},{"name":"CARID, Cardiovascular Research Institute D\u00fcsseldorf (A.P., M.G., D.J.G., M.A., M.P., R.S., S.H., J.M., S.G., M. Kelm, A.G., U.F., J.W.F.), University Hospital, Heinrich-Heine-University D\u00fcsseldorf, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.","family":"Gorski","sequence":"additional","affiliation":[{"name":"From the Institut f\u00fcr Pharmakologie und Klinische Pharmakologie (A.P., M.G., D.J.G., M.A., M.P., R.S., S.H., J.M., S.G., J.W.F.), University Hospital, Heinrich-Heine-University D\u00fcsseldorf, Germany"},{"name":"CARID, Cardiovascular Research Institute D\u00fcsseldorf (A.P., M.G., D.J.G., M.A., M.P., R.S., S.H., J.M., S.G., M. 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