Circulation Research. 2001;89:168-173
Published online before print July 5, 2001, doi: 10.1161/hh1401.093314
Published online before print July 5, 2001, doi: 10.1161/hh1401.093314
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© 2001 American Heart Association, Inc.
Integrative Physiology |
Cardiac-Specific Expression of Heme Oxygenase-1 Protects Against Ischemia and Reperfusion Injury in Transgenic Mice
From the Cardiovascular (S.-F.Y., R.T., M.D.L., Z.Y.W., K.M., M.S., B.I., J.S.I., M.-E.L., M.A.P.) and Pulmonary and Critical Care (M.D.L, M.A.P.) Divisions and the Department of Medicine (S.-F.Y., R.T., M.D.L., L.G.M, L.Z., J.S.I., V.J.D., M.-E.L., M.A.P), Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass.
Correspondence to Shaw-Fang Yet, PhD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Thorn 1127, Boston, MA 02115. E-mail syet{at}rics.bwh.harvard.edu
Abstract— Heme oxygenase (HO)-1 degrades the pro-oxidant heme and generates carbon monoxide and antioxidant bilirubin. We have previously shown that in response to hypoxia, HO-1–null mice develop infarcts in the right ventricle of their hearts and that their cardiomyocytes are damaged by oxidative stress. To test whether HO-1 protects against oxidative injury in the heart, we generated cardiac-specific transgenic mice overexpressing different levels of HO-1. By use of a Langendorff preparation, hearts from transgenic mice showed improved recovery of contractile performance during reperfusion after ischemia in an HO-1 dose–dependent manner. In vivo, myocardial ischemia and reperfusion experiments showed that infarct size was only 14.7% of the area at risk in transgenic mice compared with 56.5% in wild-type mice. Hearts from these transgenic animals had reduced inflammatory cell infiltration and oxidative damage. Our data demonstrate that overexpression of HO-1 in the cardiomyocyte protects against ischemia and reperfusion injury, thus improving the recovery of cardiac function.
Key Words: heart • infarction • Langendorff preparation • cytoprotection • inflammation
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