Direct intra-cardiomuscular transfer of β2-adrenergic receptor gene augments cardiac output in cardiomyopathic hamsters View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2000-12

AUTHORS

K Tomiyasu, Y Oda, M Nomura, E Satoh, S Fushiki, J Imanishi, M Kondo, O Mazda

ABSTRACT

In chronic heart failure, down-regulation of beta-adrenergic receptor (beta-AR) occurs in cardiomyocytes, resulting in low catecholamine response and impaired cardiac function. To correct the irregularity in the beta-AR system, beta-AR gene was transduced in vivo into failing cardiomyocytes. The Epstein-Barr virus (EBV)-based plasmid vector carrying human beta2-AR gene was injected into the left ventricular muscle of Bio14.6 cardiomyopathic hamsters whose beta-AR is down-regulated in the cardiomyocytes. The echocardiographic examinations revealed that stroke volume (SV) and cardiac output (CO) were significantly elevated at 2 to 4 days after the beta2-AR gene transfer. Systemic loading of isoproterenol increased the cardiac parameters more significantly on day 2 to day 7, indicating that the adrenergic response was augmented by the genetic transduction. The same procedure did not affect the cardiac function of normal hamsters. Immunohistochemical examinations demonstrated human beta2-AR expression in failing cardiomyocytes transduced with the gene. RT-PCR analysis detected mRNA for the transgene in the heart but not in the liver, spleen, or kidney. The procedures may provide a feasible strategy for gene therapy of severe heart failure. Gene Therapy (2000) 7, 2087-2093. More... »

PAGES

3301329

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.gt.3301329

DOI

http://dx.doi.org/10.1038/sj.gt.3301329

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045917282

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11223989


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