Journal
CIRCULATION RESEARCH
Volume 89, Issue 2, Pages 168-173Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/hh1401.093314
Keywords
heart; infarction; Langendorff preparation; cytoprotection; inflammation
Funding
- NHLBI NIH HHS [HL-57977, HL-60788, HL-10113] Funding Source: Medline
- NIGMS NIH HHS [GM-53249] Funding Source: Medline
Ask authors/readers for more resources
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 mess. 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available