Proteomic analysis of short-term preload-induced eccentric cardiac hypertrophy
2016 | journal article; research paper. A publication with affiliation to the University of Göttingen.
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Proteomic analysis of short-term preload-induced eccentric cardiac hypertrophy
Mohamed, B. A. ; Asif, A. R. ; Schnelle, M. ; Qasim, M.; Khadjeh, S. ; Lbik, D. & Schott, P. et al. (2016)
Journal of Translational Medicine, 14 art. 149. DOI: https://doi.org/10.1186/s12967-016-0898-5
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- Authors
- Mohamed, Belal A. ; Asif, Abdul R. ; Schnelle, Moritz ; Qasim, Mohamed; Khadjeh, Sara ; Lbik, Dawid; Schott, Peter ; Hasenfuß, Gerd ; Toischer, Karl
- Abstract
- Background: Hemodynamic load leads to cardiac hypertrophy and heart failure. While afterload (pressure overload) induces concentric hypertrophy, elevation of preload (volume overload) yields eccentric hypertrophy and is associated with a better outcome. Here we analysed the proteomic pattern of mice subjected to short-term preload. Methods and Results: Female FVB/N mice were subjected to aortocaval shunt-induced volume overload that leads to an eccentric hypertrophy (left ventricular weight/tibia length +31 %) with sustained systolic heart function at 1 week after operation. Two-dimensional gel electrophoresis (2-DE) followed by mass spectrometric analysis showed alteration in the expression of 25 protein spots representing 21 different proteins. 64 % of these protein spots were up-regulated and 36 % of the protein spots were consistently down-regulated. Interestingly, alpha-1-antitrypsin was down-regulated, indicating higher elastin degradation and possibly contributing to the early dilatation. In addition to contractile and mitochondrial proteins, polymerase I and transcript release factor protein (PTRF) was also up-regulated, possibly contributing to the preload-induced signal transduction. Conclusions: Our findings reveal the proteomic changes of early-stage eccentric myocardial remodeling after volume overload. Induced expression of some of the respiratory chain enzymes suggests a metabolic shift towards an oxidative phosphorylation that might contribute to the favorable remodeling seen in early VO. Down-regulation of alpha-1-antitrypsin might contribute to extracellular matrix remodeling and left ventricular dilatation. We also identified PTRF as a potential signaling regulator of volume overload-induced cardiac hypertrophy.
- Issue Date
- 2016
- Publisher
- Biomed Central Ltd
- Journal
- Journal of Translational Medicine
- ISSN
- 1479-5876