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Adenoviral gene transfer of Akt enhances myocardial contractility and intracellular calcium handling (118 visite)

Cittadini A, Monti MG, Iaccarino G, Di Rella F, Tsichlis PN, Di Gianni A, Strömer H, Sorriento D, Peschle C, Trimarco B, Saccà L, Condorelli G

Gene Ther Gene Therapy (ISSN: 0969-7128), 2006; 13(1): 8-19.

Tipo di articolo: Journal Article, , Impact factor: 4.782, Impact factor a 5 anni: 3.67, Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-29244470231&partnerID=40&md5=2d35430a993bef9415a2b220a3bf1830

Parole chiave: Akt, Calcium, Heart, Oxygen Consumption, Adenosine Triphosphatase (calcium), Adenovirus Vector, Adenylate Cyclase, Aequorin, Beta Adrenergic Receptor, Buffer, Calsequestrin, Dobutamine, Messenger Rna, Phospholamban, Protein Kinase B, Ryanodine Receptor, Animal Experiment, Animal Tissue, Aorta Clamping, Article, Binding Affinity, Body Weight, Calcium Cell Level, Calcium Transport, Catheter, Cell Energy, Controlled Study, Documentation, Enzyme Activity, Gene Transfer, Heart Hypertrophy, Heart Left Ventricle, Heart Left Ventricle Contractility, Heart Left Ventricle Mass, Heart Muscle Contractility, Heart Muscle Oxygen Consumption, Heart Perfusion, Heart Ventricle Pressure, Inotropism, Isolated Heart, Myofilament, Nonhuman, Postoperative Period, Pressure Gradient, Priority Journal, Protein Content, Rat Strain, Receptor Density, Sarcoplasmic Reticulum, Steady State, Systole, Tetany, Titrimetry, Viral Gene Delivery System, Wild Type, Adenoviridae, Adrenergic Beta-Agonists, Calcium-Transporting Atpases, Echocardiography, Gene Therapy, Genetic Vectors, Heart Failure, Congestive, Myocardial Contraction, Myocardial Reperfusion Injury, Ng-Nitroarginine Methyl Ester, Nitric Oxide Synthase, Proto-Oncogene Proteins C-Akt, Sprague-Dawley, Transduction,

Affiliazioni: *** IBB - CNR ***
Department of Clinical Medicine and Cardiovascular Sciences, University 'Federico II', Via S Pansini 5, Naples 80131, Italy
Molecular Oncology Research Institute, New England Medical Center, Boston, MA, United States
Medizinische Universitätsklinik, Würzburg, Germany
Instituto Superiore Sanita', Rome, Italy
San Raffaele Biomedical Science Park, Rome-Multimedica Hospital, Milan, Italy
Institute of Molecular Medicine, University of California, San Diego, CA, United States

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The serine-threonine kinase Akt/PKB mediates stimuli from different classes of cardiomyocyte receptors, including the growth hormone/insulin like growth factor and the β-adrenergic receptors. Whereas the growth-promoting and antiapoptotic properties of Akt activation are well established, little is known about the effects of Akt on myocardial contractility, intracellular calcium (Ca2+) handling, oxygen consumption, and β-adrenergic pathway. To this aim, Sprague -Dawley rats were subjected to a wild-type Akt in vivo adenoviral gene transfer using a catheter-based technique combined with aortopulmonary crossclamping. Left ventricular (LV) contractility and intracellular Ca2+ handling were evaluated in an isolated isovolumic buffer-perfused, aequorin-loaded whole heart preparations 10 days after the surgery. The Ca2+-force relationship was obtained under steady-state conditions in tetanized muscles. No significant hypertrophy was detected in adenovirus with wild-type Akt (Ad.Akt) versus controls rats (LV-to-body weight ratio 2.6±177;0.2 versus 2.7±177;0.1mg/g, controls versus Ad.Akt, P, NS). LV contractility, measured as developed pressure, increased by 41% in Ad.Akt. This was accounted for by both more systolic Ca2+ available to the contractile machinery (+19% versus controls) and by enhanced myofilament Ca2+ responsiveness, documented by an increased maximal Ca2+-activated pressure (+19% versus controls) and a shift to the left of the Ca2+-force relationship. Such increased contractility was paralleled by a slight increase of myocardial oxygen consumption (14%), while titrated dose of dobutamine providing similar inotropic effect augmented oxygen consumption by 39% (P
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Ciampi Q, Betocchi S, Losi MA, Ferro A, Cuocolo A, Lombardi R, Villari B, Chiariello M
* Abnormal blood-pressure response to exercise and oxygen consumption in patients with hypertrophic cardiomyopathy (79 visite)
J Nucl Cardiol (ISSN: 1532-6551, 1071-3581, 1532-6551electronic), 2007 Nov; 14(6): 869-875.
Impact Factor: 2.359
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1 Records (1 escludendo Abstract e Conferenze).
Impact factor totale: 2.359 (2.359 escludendo Abstract e Conferenze).
Impact factor a 5 anni totale: 2.269 (2.269 escludendo Abstract e Conferenze).

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