Expression and Protective Role of Heme Oxygenase-1 in Delayed Myocardial Preconditioning.
From: Department of Surgical Research and Techniques, University of Pécs, Medical Faculty, Kodaly Zoltan St. 20, Pécs, H-7624 Hungary. jancsogabor@hotmail.com
Annals of the New York Academy of Sciences
- Publish Date: Jan 2007
- ISSN: 0077-8923
- Volume: 1095
- Issue:
- Pages: 251-61
- Medium: Print
- Language: English
- Citation (JAMA): Jancsó Gábor, Cserepes Barbara, Gasz Balázs, et al. Expression and Protective Role of Heme Oxygenase-1 in Delayed Myocardial Preconditioning.. Ann. N. Y. Acad. Sci. Jan 2007;1095:251-61
Abstract
In the study the authors aimed to demonstrate the expression and protective effect of heme oxygenase-1 (HO-1) in the delayed preconditioning (PC) on cultured myocardiac cells. Neonatal rat cardiac myocytes were exposed to ischemic (ischemic medium [IM] for 20 min) and pharmacological (adenosine, epinephrine, opioid) PC. Twenty-four hours later cells were subjected to a simulated ischemia (SI) — culturing for 3 h in IM, followed by 2-h reperfusion in normal medium — and then lactate dehydrogenase (LDH), live/death ratio, and apoptosis were measured. For demonstrating the protective role of HO-1, its enzymatic activity was competitively inhibited by administration of zinc protoporphyrin IX (ZnPPIX), and HO-1 synthesis was blocked with HO-1 siRNA. Cells in control group were cultured under normoxic conditions. In SI group, cells underwent only an SI without PC. HO-1 expression in all of the groups was demonstrated with immunostaining. Our results showed a significant decrease of LDH release, apoptosis, and cell death in PC groups versus SI group, which has been risen in ZnPPIX- and HO-1 siRNA-treated groups. HO-1 immunostaining showed an appreciable HO-1 expression in PC groups, which was abolished with HO-1 siRNA administration, but not in ZnPPIX group. The results therefore suggest that HO-1 expression increases in both ischemic and pharmacological PC, and HO-1 has cellular protective effect against cell death and apoptosis in ischemia-reperfusion-induced oxidative injury.
Mesh Headings (Keywords): Animals, Animals, Newborn, Cells, Cultured, Heme Oxygenase-1, Ischemic Preconditioning, Myocardial, Myocardium, Rats, Rats, Wistar
Check for Full Text / PubMed Unique Identifier (PMID): 17404038
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.