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Verfasst von:Buß, Sebastian Johannes [VerfasserIn]   i
 Riffel, Johannes [VerfasserIn]   i
 Malekar, Pratima [VerfasserIn]   i
 Hagenmüller, Marco [VerfasserIn]   i
 Zhang, Min [VerfasserIn]   i
 Weiss, Celine [VerfasserIn]   i
 Katus, Hugo [VerfasserIn]   i
 Hardt, Stefan [VerfasserIn]   i
Titel:Chronic Akt blockade aggravates pathological hypertrophy and inhibits physiological hypertrophy
Verf.angabe:Sebastian J. Buss, Johannes H. Riffel, Pratima Malekar, Marco Hagenmueller, Christina Asel, Min Zhang, Celine Weiss, Hugo A. Katus, and Stefan E. Hardt
Jahr:2012
Jahr des Originals:2011
Umfang:11 S.
Fussnoten:Gesehen am 25.05.2018 ; First published November 11, 2011
Titel Quelle:Enthalten in: American journal of physiology / Heart and circulatory physiology
Ort Quelle:Bethesda, Md. : American Physiological Society, 1977
Jahr Quelle:2012
Band/Heft Quelle:302(2012), 2, Seite H420-H430
ISSN Quelle:1522-1539
Abstract:The attenuation of adverse myocardial remodeling and pathological left ventricular (LV) hypertrophy is one of the hallmarks for improving the prognosis after myocardial infarction (MI). The protein kinase Akt plays a central role in regulating cardiac hypertrophy, but the in vivo effects of chronic pharmacological inhibition of Akt are unknown. We investigated the effect of chronic Akt blockade with deguelin on the development of pathological [MI and aortic banding (AB)] and physiological (controlled treadmill running) hypertrophy. Primary cardiomyocyte cultures were incubated with 10 μmol deguelin for 48 h, and Wistar rats were treated orally with deguelin (4.0 mg·kg−1·day−1) for 4 wk starting 1 day after the induction of MI or AB. Exercise-trained animals received deguelin for 4 wk during the training period. In vitro, we observed reduced phosphorylation of Akt and glycogen synthase kinase (GSK)-3β after an incubation with deguelin, whereas MAPK signaling was not significantly affected. In vivo, treatment with deguelin led to attenuated phosphorylation of Akt and GSK-3β 4 wk after MI. These animals showed significantly increased heart weights and impaired LV function with increased end-diastolic diameters (12.0 ± 0.3 vs. 11.1 ± 0.3 mm, P < 0.05), end-diastolic volumes (439 ± 8 vs. 388 ± 18 μl, P < 0.05), and cardiomyocyte sizes (+20%, P < 0.05) compared with MI animals receiving vehicle treatment. Furthermore, activation of Ca2+/calmodulin-dependent kinase II in deguelin-treated MI animals was increased compared with the vehicle-treated group. Four wk after AB, we observed an augmentation of pathological hypertrophy in the deguelin-treated group with a significant increase in heart weights and cardiomyocyte sizes (>20%, P < 0.05). In contrast, the development of physiological hypertrophy was inhibited by deguelin treatment in exercise-trained animals. In conclusion, chronic Akt blockade with deguelin aggravates adverse myocardial remodeling and antagonizes physiological hypertrophy.
DOI:doi:10.1152/ajpheart.00211.2011
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: http://dx.doi.org/10.1152/ajpheart.00211.2011
 Volltext: https://www.physiology.org/doi/10.1152/ajpheart.00211.2011
 DOI: https://doi.org/10.1152/ajpheart.00211.2011
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1575523159
Verknüpfungen:→ Zeitschrift

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