Activation of myocardial angiogenesis and upregulation of fibroblast growth factor-2 in transmyocardial-revascularization-treated mice
Autor: | Choo Sj, Coffin Jd, Duran Cm, Grass Tm, Reichert C, Martin Sl, Kami E. Chiotti |
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Rok vydání: | 2000 |
Předmět: |
Vascular Endothelial Growth Factor A
medicine.medical_specialty Angiogenesis medicine.medical_treatment VEGF receptors Neovascularization Physiologic Endothelial Growth Factors Fibroblast growth factor Mice Downregulation and upregulation Internal medicine medicine Myocardial Revascularization Animals Lymphokines Wound Healing biology business.industry Vascular Endothelial Growth Factors Growth factor Myocardium Heart General Medicine Transmyocardial revascularization Immunohistochemistry Up-Regulation Endocrinology biology.protein Fibroblast Growth Factor 2 Cardiology and Cardiovascular Medicine business Endothelial Cell Growth Factor |
Zdroj: | Coronary artery disease. 11(7) |
ISSN: | 0954-6928 |
Popis: | OBJECTIVE To evaluate the growth factor responses associated with myocardial angiogenesis. DESIGN Mice were treated with transmyocardial revascularization (TMR) and evaluated for angiogenic and growth factor responses. METHODS TMR was performed via thoractomy with a 27 g needle. At 2, 5, and 7 days post-treatment, hearts were removed from the TMR treated and control groups, then assayed for angiogenesis, fibroblast growth factor (FGF)-2 expression and vascular endothelial cell growth factor (VEGF) expression. RESULTS TMR caused an angiogenic reaction in the myocardial blood vessels at 7 days post-TMR treatment. Elevated FGF-2 corresponded with increased TMR related angiogenesis. VEGF levels only increased in hearts that were prewounded then TMR treated. CONCLUSIONS The data show that TMR stimulates myocardial angiogenesis. The angiogenic reaction is mediated by FGF-2 which increased in most experimental treatment groups. The VEGF response was more specific, requiring prewounding then TMR treatment for a VEGF increase. |
Databáze: | OpenAIRE |
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