Published January 1, 2010
| Version v1
Journal article
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Biglycan protects cardiomyocytes against hypoxia/reoxygenation injury: Role of nitric oxide
Creators
- 1. Biol Res Ctr, Lab Anim Genet & Mol Neurobiol, Inst Biochem, H-6701 Szeged, Hungary
- 2. Univ Szeged, Cardiovasc Res Grp, Dept Biochem, H-6720 Szeged, Hungary
- 3. Univ Szeged, Inst Pharmaceut Chem, H-6720 Szeged, Hungary
Description
Biglycan, a proteoglycan component of extracellular matrix, has been suspected to contribute to the development of atherosclerosis, but overexpression of biglycan in transgenic mice has been shown to induce cardioprotective genes including nitric oxide (NO) synthases in the heart. Therefore, here we hypothesized if exogenous administration of biglycan exerts cytoprotection. Primary cardiomyocytes from neonatal rats were subjected to 150 min hypoxia and 2 h reoxygenation. Mortality of cardiomyocytes was dose-dependently attenuated by pretreatment with 1-100 nM biglycan. Biglycan enhanced eNOS mRNA and protein, and significantly increased NO content of cardiomyocytes. The NO synthase inhibitor L-nitro-arginine-methyl-ester significantly attenuated the cytoprotective effect of biglycan. This is the first demonstration that biglycan leads to cytoprotection against hypoxia/reoxygenation injury, and that this phenomenon is partially mediated by an NO-dependent mechanism. (c) 2010 Elsevier Ltd. All rights reserved.
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