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Myocardial angiogenesis after plasmid or adenoviral VEGF-A(165) gene transfer in rat myocardial infarction model
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2007 (English)In: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, Vol. 73, no 3, 481-487 p.Article in journal (Refereed) Published
Abstract [en]

Objective: To compare gene transfer of plasmid (P) and adenovirus (Ad) encoding human vascular endothelial growth factor-A(165) (hVEGF-A(165)) angiogenic efficacy and adverse effects as regards apoptosis and ectopic expression of the transgene in a rat myocardial infarction model. Methods: Myocardial infarction was provoked in Fisher rats. One week later, PhVEGF-A(165), PLacZ, AdhVEGF-A(165), or AdLacZ was transferred intramyocardially along the border of the myocardial infarction. hVEGF-A expression was detected with ELISA. Myocardial vessel density was analyzed 1 and 4 weeks after gene transfer. Apoptosis was detected by TUNEL staining. Cardiac function was assessed with Tissue Doppler Velocity Imaging. Results: Although AdhVEGF-A(165) had substantially higher myocardial hVEGF-A expression than PhVEGF-A(165), AdhVEGF-A(165) and PhVEGF-A(165) induced angiogenic effects to a similar extent with maintained increased arteriolar density after 4 weeks of gene transfer (p < 0.05). The two treatments also improved left ventricular function similarly. Adenoviral gene transfer induced a higher number of TUNEL positive cells than plasmid (p < 0.02). Ectopic expression of the transgene was present with both vectors but substantially higher after adenoviral gene transfer. Conclusions: AdhVEGF-A165 has no obvious angiogenic advantage over PhVEGF-A165 but more side effects at least in a rat myocardial infarction model. This indicates that PhVEGF-A(165) might be more applicable for therapeutic angiogenesis than AdhVEGF-A(165).

Place, publisher, year, edition, pages
2007. Vol. 73, no 3, 481-487 p.
Keyword [en]
angiogenesis, gene therapy, infarction, growth factors, apoptosis, endothelial growth-factor, expression, ischemia, vectors, feasibility, mechanisms, apoptosis, therapy, artery, trial
National Category
Medical and Health Sciences
URN: urn:nbn:se:kth:diva-16381DOI: 10.1016/j.cardiores.2006.10.011ISI: 000244164100008OAI: diva2:334423
QC 20100525Available from: 2010-08-05 Created: 2010-08-05 Last updated: 2012-03-23Bibliographically approved

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Brodin, Lars-Åke
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