{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T02:59:05Z","timestamp":1788317945317,"version":"build-2803163510"},"reference-count":72,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,1,23]]},"abstract":"\n Background<\/jats:title>\n \n During myocardial ischemia\/reperfusion (\n MI<\/jats:styled-content>\n \/R) injury, there is extensive release of immunogenic metabolites that activate cells of the innate immune system. These include\n ATP<\/jats:styled-content>\n and\n AMP<\/jats:styled-content>\n , which upregulate chemotaxis, migration, and effector function of early infiltrating inflammatory cells. These cells subsequently drive further tissue devitalization. Mesenchymal stromal cells (\n MSC<\/jats:styled-content>\n s) are a potential treatment modality for\n MI<\/jats:styled-content>\n \/R because of their powerful anti\u2010inflammatory capabilities; however, the manner in which they regulate the acute inflammatory milieu requires further elucidation.\n CD<\/jats:styled-content>\n 73, an ecto\u20105\u2032\u2010nucleotidase, may be critical in regulating inflammation by converting pro\u2010inflammatory\n AMP<\/jats:styled-content>\n to anti\u2010inflammatory adenosine. We hypothesized that\n MSC<\/jats:styled-content>\n \u2010mediated conversion of\n AMP<\/jats:styled-content>\n into adenosine reduces inflammation in early\n MI<\/jats:styled-content>\n \/R, favoring a micro\u2010environment that attenuates excessive innate immune cell activation and facilitates earlier cardiac recovery.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n Adult rats were subjected to 30\u00a0minutes of\n MI<\/jats:styled-content>\n \/R injury.\n MSC<\/jats:styled-content>\n s were encapsulated within a hydrogel vehicle and implanted onto the myocardium. A subset of\n MSC<\/jats:styled-content>\n s were pretreated with the\n CD<\/jats:styled-content>\n 73 inhibitor, \u03b1,\u03b2\u2010methylene adenosine diphosphate, before implantation. Using liquid chromatography\/mass spectrometry, we found that\n MSC<\/jats:styled-content>\n s increase myocardial adenosine availability following injury via\n CD<\/jats:styled-content>\n 73 activity.\n MSC<\/jats:styled-content>\n s also reduce innate immune cell infiltration as measured by flow cytometry, and hydrogen peroxide formation as measured by Amplex Red assay. These effects were dependent on\n MSC<\/jats:styled-content>\n \u2010mediated\n CD<\/jats:styled-content>\n 73 activity. Finally, through echocardiography we found that\n CD<\/jats:styled-content>\n 73 activity on\n MSC<\/jats:styled-content>\n s was critical to optimal protection of cardiac function following\n MI<\/jats:styled-content>\n \/R injury.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n MSC<\/jats:styled-content>\n \u2010mediated conversion of\n AMP<\/jats:styled-content>\n to adenosine by\n CD<\/jats:styled-content>\n 73 exerts a powerful anti\u2010inflammatory effect critical for cardiac recovery following\n MI<\/jats:styled-content>\n \/R injury.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.117.006949","type":"journal-article","created":{"date-parts":[[2018,1,13]],"date-time":"2018-01-13T20:10:24Z","timestamp":1515874224000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":48,"title":["Adenosine Production by Biomaterial\u2010Supported Mesenchymal Stromal Cells Reduces the Innate Inflammatory Response in Myocardial Ischemia\/Reperfusion Injury"],"prefix":"10.1161","volume":"7","author":[{"given":"Eric Y.","family":"Shin","sequence":"first","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lanfang","family":"Wang","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marina","family":"Zemskova","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]},{"name":"University of Arizona","place":["Tucson"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juline","family":"Deppen","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai","family":"Xu","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]},{"name":"Xiangya Hospital of Central South University","place":["Changsha, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederick","family":"Strobel","sequence":"additional","affiliation":[{"name":"Emory University","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andr\u00e9s J.","family":"Garc\u00eda","sequence":"additional","affiliation":[{"name":"Georgia Institute of Technology","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rabindra","family":"Tirouvanziam","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca D.","family":"Levit","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"92","DOI":"10.1172\/JCI62874","article-title":"Myocardial ischemia\u2010reperfusion injury: a neglected therapeutic target","volume":"123","author":"Hausenloy DJ","year":"2013","unstructured":"Hausenloy DJ, Yellon DM. 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