Cardiac effects of attenuating Gsα: dependent signaling
Aims Inhibition of β-adrenergic signalling plays a key role in treatment of heart failure. Gsα is essential for β-adrenergic signal transduction. In order to reduce side-effects of beta-adrenergic inhibition diminishing β-adrenergic signalling in the heart at the level of Gsα is a promising option....
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| Hauptverfasser: | , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
January 26, 2016
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| In: |
PLOS ONE
Year: 2016, Jahrgang: 11, Heft: 1 |
| ISSN: | 1932-6203 |
| DOI: | 10.1371/journal.pone.0146988 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1371/journal.pone.0146988 Verlag, lizenzpflichtig, Volltext: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146988 
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| Verfasserangaben: | Marcus R. Streit, Celine S. Weiss, Sören Meyer, Marco M. Ochs, Marco Hagenmueller, Johannes H. Riffel, Sebastian J. Buss, Thomas Heger, Hugo A. Katus, Stefan E. Hardt |
MARC
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| 245 | 1 | 0 | |a Cardiac effects of attenuating Gsα |b dependent signaling |c Marcus R. Streit, Celine S. Weiss, Sören Meyer, Marco M. Ochs, Marco Hagenmueller, Johannes H. Riffel, Sebastian J. Buss, Thomas Heger, Hugo A. Katus, Stefan E. Hardt |
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| 520 | |a Aims Inhibition of β-adrenergic signalling plays a key role in treatment of heart failure. Gsα is essential for β-adrenergic signal transduction. In order to reduce side-effects of beta-adrenergic inhibition diminishing β-adrenergic signalling in the heart at the level of Gsα is a promising option. Methods and Results We analyzed the influence of Gsα on regulation of myocardial function and development of cardiac hypertrophy, using a transgenic mouse model (C57BL6/J mice) overexpressing a dominant negative Gsα-mutant under control of the α-MHC-promotor. Cardiac phenotype was characterized in vivo and in vitro and under acute and chronic β-adrenergic stimulation. At rest, Gsα-DN-mice showed bradycardia (602 ± 13 vs. 660 ± 17 bpm, p<0.05) and decreased dp/dtmax (5037 ± 546- vs. 6835 ± 505 mmHg/s, p = 0.02). No significant differences were found regarding ejection fraction, heart weight and cardiomyocyte size. β-blockade by propranolol revealed no baseline differences of hemodynamic parameters between wildtype and Gsα-DN-mice. Acute adrenergic stimulation resulted in decreased β-adrenergic responsiveness in Gsα-DN-mice. Under chronic adrenergic stimulation, wildtype mice developed myocardial hypertrophy associated with increase of LV/BW-ratio by 23% (4.4 ± 0.2 vs. 3.5 ± 0.1 mg/g, p<0.01) and cardiac myocyte size by 24% (14927 ± 442 px vs. 12013 ± 583 px, p<0.001). In contrast, both parameters were unchanged in Gsα-DN-mice after chronic isoproterenol stimulation. Conclusion Overexpression of a dominant negative mutant of Gsα leads to decreased β-adrenergic responsiveness and is protective against isoproterenol-induced hypertrophy. Thus, Gsα-DN-mice provide novel insights into β-adrenergic signal transduction and its modulation in myocardial overload and failure. | ||
| 650 | 4 | |a G-protein signaling | |
| 650 | 4 | |a Genetically modified animals | |
| 650 | 4 | |a Heart | |
| 650 | 4 | |a Heart failure | |
| 650 | 4 | |a Heart rate | |
| 650 | 4 | |a Hyperexpression techniques | |
| 650 | 4 | |a Isoproterenol | |
| 650 | 4 | |a Mouse models | |
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