We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
Inhibition of TGF-beta1 signaling by eNOS gene transfer improves ventricular remodeling after myocardial infarction through angiogenesis and reduction of apoptosis.
Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology 2007 July
INTRODUCTION: Endothelial nitric oxide synthase and nitric oxide have been implicated in protection against myocardial ischemia injury. However, the angiogenic effect of endothelial nitric oxide synthase on infarcted myocardium and the role of tumor growth factor beta1 signaling in cardiac remodeling mediated by endothelial nitric oxide synthase/nitric oxide have not yet been elucidated.
METHODS: Human endothelial nitric oxide synthase gene in an adenovirus vector was delivered locally into rat heart 4 days prior to the induction of myocardial infarction by left anterior descending coronary artery ligation. Cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and neovascularization was identified immunohistochemically.
RESULTS: Endothelial nitric oxide synthase gene transfer significantly reduced infarct size and improved cardiac contractility and left ventricular diastolic function at 24 h after myocardial infarction. In addition, endothelial nitric oxide synthase significantly reduced myocardial-infarction-induced cardiomyocyte apoptosis. Activation of tumor growth factor beta1 and Smad-2 after myocardial infarction was also dramatically reduced by endothelial nitric oxide synthase. Moreover, the deterioration of both systolic and diastolic functions, in conjunction with thin left ventricular remodeling at 7 days after myocardial infarction, was prevented by endothelial nitric oxide synthase. Capillary density, as identified by alpha-smooth muscle actin immunostaining, was significantly increased in the infarcted myocardium after endothelial nitric oxide synthase transfer compared with myocardial infarction control. All cardioprotective effects of endothelial nitric oxide synthase were blocked by N(omega)-nitro-l-arginine methyl ester administration, indicating a nitric-oxide-mediated event.
CONCLUSION: These results demonstrate that the endothelial nitric oxide synthase/nitric oxide system provides cardiac protection after myocardial infarction injury through inhibition of cardiac apoptosis, stimulation of neovascularization, and suppression of tumor growth factor beta1/Smad-2 signaling.
METHODS: Human endothelial nitric oxide synthase gene in an adenovirus vector was delivered locally into rat heart 4 days prior to the induction of myocardial infarction by left anterior descending coronary artery ligation. Cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and neovascularization was identified immunohistochemically.
RESULTS: Endothelial nitric oxide synthase gene transfer significantly reduced infarct size and improved cardiac contractility and left ventricular diastolic function at 24 h after myocardial infarction. In addition, endothelial nitric oxide synthase significantly reduced myocardial-infarction-induced cardiomyocyte apoptosis. Activation of tumor growth factor beta1 and Smad-2 after myocardial infarction was also dramatically reduced by endothelial nitric oxide synthase. Moreover, the deterioration of both systolic and diastolic functions, in conjunction with thin left ventricular remodeling at 7 days after myocardial infarction, was prevented by endothelial nitric oxide synthase. Capillary density, as identified by alpha-smooth muscle actin immunostaining, was significantly increased in the infarcted myocardium after endothelial nitric oxide synthase transfer compared with myocardial infarction control. All cardioprotective effects of endothelial nitric oxide synthase were blocked by N(omega)-nitro-l-arginine methyl ester administration, indicating a nitric-oxide-mediated event.
CONCLUSION: These results demonstrate that the endothelial nitric oxide synthase/nitric oxide system provides cardiac protection after myocardial infarction injury through inhibition of cardiac apoptosis, stimulation of neovascularization, and suppression of tumor growth factor beta1/Smad-2 signaling.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app