Cardiac-specific expression of heme oxygenase-1 protects against ischemia and reperfusion injury in transgenic mice.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Yet, SF; Tian, R; Layne, MD; Wang, ZY; Maemura, K; Solovyeva, M; Ith, B; Melo, LG; Zhang, L; Ingwall, JS; Dzau, VJ; Lee, ME; Perrella, MA

Published Date

  • July 20, 2001

Published In

Volume / Issue

  • 89 / 2

Start / End Page

  • 168 - 173

PubMed ID

  • 11463724

Pubmed Central ID

  • 11463724

Electronic International Standard Serial Number (EISSN)

  • 1524-4571

Language

  • eng

Conference Location

  • United States