Cardiac-specific expression of heme oxygenase-1 protects against ischemia and reperfusion injury in transgenic mice.
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.
Duke Scholars
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- Myocardium
- Myocardial Reperfusion Injury
- Myocardial Ischemia
- Myocardial Infarction
- Mice, Transgenic
- Mice
- Membrane Proteins
- Humans
- Heme Oxygenase-1
- Heme Oxygenase (Decyclizing)
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Myocardium
- Myocardial Reperfusion Injury
- Myocardial Ischemia
- Myocardial Infarction
- Mice, Transgenic
- Mice
- Membrane Proteins
- Humans
- Heme Oxygenase-1
- Heme Oxygenase (Decyclizing)