{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,26]],"date-time":"2026-07-26T00:12:54Z","timestamp":1785024774857,"version":"3.55.0"},"reference-count":66,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2014,1,27]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The core region of a myocardial infarction is notoriously unsupportive of cardiomyocyte survival. However, there has been less investigation of the potentially beneficial spontaneous recruitment of endogenous bone marrow progenitor cells (\n              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              s) within infarcted areas. In the current study we examined the role of tissue oxygenation and derived toxic species in the control of\n              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              engraftment during postinfarction heart remodeling.\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              For assessment of cellular origin, local oxygenation, redox status, and fate of cells in the infarcted region, myocardial infarction in mice with or without LacZ\n              <jats:sup>+<\/jats:sup>\n              bone marrow transplantation was induced by coronary ligation. Sham\u2010operated mice served as controls. After 1\u00a0week, LacZ\n              <jats:sup>+<\/jats:sup>\n              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              \u2010derived cells were found inhomogeneously distributed into the infarct zone, with a lower density at its core. Electron paramagnetic resonance (EPR) oximetry showed that\n              <jats:styled-content style=\"fixed-case\">pO<\/jats:styled-content>\n              <jats:sub>2<\/jats:sub>\n              in the infarct recovered starting on day 2 post\u2013myocardial infarction, concomitant with wall thinning and erythrocytes percolating through muscle microruptures. Paralleling this reoxygenation, increased generation of reactive oxygen\/nitrogen species was detected at the infarct core. This process delineated a zone of diminished\n              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              engraftment, and at 1\u00a0week infiltrating cells displayed immunoreactive 3\u2010nitrotyrosine and apoptosis. In vivo treatment with a superoxide dismutase mimetic significantly reduced reactive oxygen species formation and amplified\n              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              accumulation. This treatment also salvaged wall thickness by 43% and left ventricular ejection fraction by 27%, with significantly increased animal survival.\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              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              engraftment in the infarct inversely mirrored the distribution of reactive oxygen\/nitrogen species. Antioxidant treatment resulted in increased numbers of engrafted\n              <jats:styled-content style=\"fixed-case\">BMPC<\/jats:styled-content>\n              s, provided functional protection to the heart, and decreased the incidence of myocardial rupture and death.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.113.000471","type":"journal-article","created":{"date-parts":[[2014,1,14]],"date-time":"2014-01-14T04:54:18Z","timestamp":1389675258000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":7,"title":["Reoxygenation\u2010Derived Toxic Reactive Oxygen\/Nitrogen Species Modulate the Contribution of Bone Marrow Progenitor Cells to Remodeling After Myocardial Infarction"],"prefix":"10.1161","volume":"3","author":[{"given":"Nicanor I.","family":"Moldovan","sequence":"first","affiliation":[{"name":"Department of Internal Medicine\/Division of Cardiovascular Medicine, The Ohio State University, 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OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fuchun","family":"Yang","sequence":"additional","affiliation":[{"name":"Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leni","family":"Moldovan","sequence":"additional","affiliation":[{"name":"Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay L.","family":"Zweier","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine\/Division of Cardiovascular Medicine, The Ohio State University, Columbus, OH"},{"name":"Davis Heart and Lung Research Institute, The Ohio State University, Columbus, 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