{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T21:49:47Z","timestamp":1768686587445,"version":"3.49.0"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2015,9,16]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Insulin\u2010like growth factor 1 (\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101) activates prosurvival pathways and improves postischemic cardiac function, but this key cytokine is not robustly expressed by cultured human cardiac stem cells. We explored the influence of an enhanced\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 paracrine signature on explant\u2010derived cardiac stem cell\u2013mediated cardiac repair.\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              Receptor profiling demonstrated that\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 receptor expression was increased in the infarct border zones of experimentally infarcted mice by 1\u00a0week after myocardial infarction. Human explant\u2010derived cells underwent somatic gene transfer to overexpress human\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 or the green fluorescent protein reporter alone. After culture in hypoxic reduced\u2010serum media, overexpression of\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 enhanced proliferation and expression of prosurvival transcripts and prosurvival proteins and decreased expression of apoptotic markers in both explant\u2010derived cells and cocultured neonatal rat ventricular cardiomyocytes. Transplant of explant\u2010derived cells genetically engineered to overexpress\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 into immunodeficient mice 1\u00a0week after infarction boosted\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 content within infarcted tissue and long\u2010term engraftment of transplanted cells while reducing apoptosis and long\u2010term myocardial scarring.\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              Paracrine engineering of explant\u2010derived cells to overexpress\n              <jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\n              \u20101 provided a targeted means of improving cardiac stem cell\u2013mediated repair by enhancing the long\u2010term survival of transplanted cells and surrounding myocardium.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.115.002104","type":"journal-article","created":{"date-parts":[[2015,9,12]],"date-time":"2015-09-12T01:43:54Z","timestamp":1442022234000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":45,"title":["Paracrine Engineering of Human Cardiac Stem Cells With Insulin\u2010Like Growth Factor 1 Enhances Myocardial Repair"],"prefix":"10.1161","volume":"4","author":[{"given":"Robyn","family":"Jackson","sequence":"first","affiliation":[{"name":"University of Ottawa Heart Institute, Ottawa, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Everad L.","family":"Tilokee","sequence":"additional","affiliation":[{"name":"University of Ottawa Heart Institute, Ottawa, 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