{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T16:58:26Z","timestamp":1777913906719,"version":"3.51.4"},"reference-count":47,"publisher":"SAGE Publications","issue":"7","license":[{"start":{"date-parts":[[2014,4,8]],"date-time":"2014-04-08T00:00:00Z","timestamp":1396915200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Toxicol Pathol"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:p>\n                    This investigation examined microRNA-208a (miR-208a) as a potential biomarker of isoproterenol (ISO)-induced cardiac injury in superoxide dismutase-2 ( Sod2\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    ) and the wild-type mice, and the potential sensitivity of Sod2\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice to ISO-induced toxicity. A single intraperitoneal injection of ISO was administered to age-matched wild-type and Sod2\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice at 0, 80, or 160 mg\/kg. Plasma miR-208a, cardiac troponin I (cTnI), and ISO systemic exposure were measured at various time points postdose. Hearts were collected for histopathology examination and for tissue expression of miR-208a and myosin heavy chain 7. ISO administration caused increases in cTnI and miR-208a plasma levels that correlated with myocardial damage; however, the magnitude of increase differed according to the types of mice. At similar ISO systemic exposure, the magnitude of cTnI was greater in wild-type mice compared to Sod2\n                    <jats:sup>+\/<\/jats:sup>\n                    <jats:sup>\u2212<\/jats:sup>\n                    mice; however, the magnitude of miR-208a was greater in Sod2\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice than that of the wild-type mice. Myocardial degeneration occurred at \u22653 hr in the wild-type and \u22656 hr in Sod2\n                    <jats:sup>+\/<\/jats:sup>\n                    <jats:sup>\u2212<\/jats:sup>\n                    mice. At \u226524 hr after ISO administration, miR-208a appeared superior to cTnI in indicating myocardial injury in both wild-type and Sod2\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice. Sod2\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice were not more sensitive than wild-type mice to ISO-induced toxicity.\n                  <\/jats:p>","DOI":"10.1177\/0192623314525684","type":"journal-article","created":{"date-parts":[[2014,4,9]],"date-time":"2014-04-09T00:36:32Z","timestamp":1397003792000},"page":"1117-1129","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":24,"title":["miR-208a as a Biomarker of Isoproterenol-induced Cardiac Injury in\n                    <i>\n                      Sod2\n                      <sup>+\/\u2212<\/sup>\n                    <\/i>\n                    and C57BL\/6J Wild-type Mice"],"prefix":"10.1177","volume":"42","author":[{"given":"Ling","family":"Liu","sequence":"first","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shirley A.","family":"Aguirre","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Winston E. N.","family":"Evering","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brad P.","family":"Hirakawa","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey R.","family":"May","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kimbie","family":"Palacio","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianying","family":"Wang","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yizhong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Bioanalytical Research, Groton, Connecticut, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory J.","family":"Stevens","sequence":"additional","affiliation":[{"name":"Pfizer Global Research and Development, Drug Safety Research and Development, San Diego, California, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2014,4,8]]},"reference":[{"key":"bibr1-0192623314525684","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2011.175919"},{"key":"bibr2-0192623314525684","doi-asserted-by":"publisher","DOI":"10.1210\/en.2007-0877"},{"key":"bibr3-0192623314525684","first-page":"821","volume":"149","author":"Bardales R. 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