Abstract | INTRODUCTION:
Vasostatin-1 (VS-1) has been suggested in protecting hypoxia/reoxygenation (H/R) injuries in isolated hearts. However, the molecular mechanisms remained to be elucidated. METHODS: RESULTS: In comparison of the blank group, cardiac myocytes overexpressing VS-1 showed significant decrease in apoptosis, intracellular oxidative stress, and inflammatory reactions (P < 0.05). In addition, serum NO concentrations and expression of eNOS were notably enhanced (P < 0.05). These protective effects of VS-1 were suppressed in the presence of apoptosis-inducing agents. CONCLUSIONS: Overexpression of VS-1 in cardiomyocytes could limit the H/R injuries at molecular levels. The protective effects were independent of endothelial cell function, suggestive of a potential therapeutic target for patients with myocardial ischemia in the future.
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Authors | Min Yu, Zheng Wang, Yue Fang, Ming-di Xiao, Zhong-xiang Yuan, Cheng-bao Lu, Lei Lin, Di-Cheng Yang |
Journal | Cardiovascular therapeutics
(Cardiovasc Ther)
Vol. 30
Issue 3
Pg. 145-51
(Jun 2012)
ISSN: 1755-5922 [Electronic] England |
PMID | 21884005
(Publication Type: Journal Article)
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Copyright | © 2011 Blackwell Publishing Ltd. |
Chemical References |
- Chromogranin A
- Enzyme Inhibitors
- Inflammation Mediators
- Peptide Fragments
- vasostatin I
- Nitric Oxide
- Malondialdehyde
- Nitric Oxide Synthase
- Superoxide Dismutase
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Topics |
- Animals
- Animals, Newborn
- Apoptosis
(drug effects)
- Blotting, Western
- Cell Survival
- Cells, Cultured
- Chromogranin A
(genetics, metabolism)
- Cytoprotection
- Endothelial Cells
(metabolism)
- Enzyme Inhibitors
(pharmacology)
- Enzyme-Linked Immunosorbent Assay
- Flow Cytometry
- Humans
- Inflammation Mediators
(metabolism)
- Malondialdehyde
(metabolism)
- Myocardial Reperfusion Injury
(genetics, metabolism, pathology, prevention & control)
- Myocytes, Cardiac
(drug effects, metabolism, pathology)
- Nitric Oxide
(metabolism)
- Nitric Oxide Synthase
(antagonists & inhibitors, metabolism)
- Oxidative Stress
- Peptide Fragments
(genetics, metabolism)
- Rats
- Rats, Sprague-Dawley
- Signal Transduction
- Superoxide Dismutase
(metabolism)
- Transfection
- Up-Regulation
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