Mediation of Cardioprotection by Transforming Growth Factor-β

Myocardial ischemia causes heart injury that is characterized by an increase in circulating tumor necrosis factor (TNF), the local production of superoxide anions, the loss of coronary vasodilation (relaxation) in response to agents that release endothelial cell relaxation factor, and cardiac tissue...

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Bibliographic Details
Published inScience (American Association for the Advancement of Science) Vol. 249; no. 4964; pp. 61 - 64
Main Authors Lefer, Allan M., Tsao, Philip, Aoki, Nobuo, Palladino, Michael A.
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for the Advancement of Science 06.07.1990
American Association for the Advancement of Science
Subjects
Acetates
Animals
Biological and medical sciences
Cardiology. Vascular system
Coronary Disease - prevention & control
Coronary heart disease
Creatine Kinase - analysis
Dose-Response Relationship, Drug
Endothelial cells
Heart
Heart - drug effects
Ischemia
Male
Medical sciences
Myocardial ischemia
Myocardial Reperfusion
Myocardium - enzymology
Myocardium - pathology
Organ Culture Techniques
Physical trauma
Rats
Rats, Inbred Strains
Superoxides
Superoxides - metabolism
Transforming Growth Factors - pharmacology
Transforming Growth Factors - therapeutic use
Tumor Necrosis Factor-alpha - pharmacology
Vasodilation - drug effects
Vasodilators
Vehicles
Human
Biochemical analysis
Ischemia
Pathophysiology
Tumor necrosis factor
Transforming growth factor
Myocardium
Cardiovascular disease
Coronary heart disease
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Summary:Myocardial ischemia causes heart injury that is characterized by an increase in circulating tumor necrosis factor (TNF), the local production of superoxide anions, the loss of coronary vasodilation (relaxation) in response to agents that release endothelial cell relaxation factor, and cardiac tissue damage. Ischemic injury can be mimicked by TNF. When given before or immediately after ischemic injury, transforming growth factor-β (TGF-β) reduced the amount of superoxide anions in the coronary circulation, maintained endothelial-dependent coronary relaxation, and reduced injury mediated by exogenous TNF. Thus, TGF-β prevented severe cardiac injury, perhaps by alleviating damage mediated by increases in circulating TNF.
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ISSN:0036-8075
1095-9203
DOI:10.1126/science.2164258