by Keyword: Myocardial infarction

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Beiert, T., Knappe, V., Tiyerili, V., Stöckigt, F., Effelsberg, V., Linhart, M., Steinmetz, M., Klein, S., Schierwagen, R., Trebicka, J., Roell, W., Nickenig, G., Schrickel, J. W., Andrié, R. P., (2018). Chronic lower-dose relaxin administration protects from arrhythmia in experimental myocardial infarction due to anti-inflammatory and anti-fibrotic properties International Journal of Cardiology 250, 21-28

Background: The peptide hormone relaxin-2 (RLX) exerts beneficial effects during myocardial ischemia, but functional data on lower-dose RLX in myocardial infarction (MI) is lacking. Therefore, we investigated the impact of 75 

Keywords: Arrhythmia, Myocardial infarction, Relaxin-2, Ventricular tachycardia

Beiert, T., Tiyerili, V., Knappe, V., Effelsberg, V., Linhart, M., Stöckigt, F., Klein, S., Schierwagen, R., Trebicka, J., Nickenig, G., Schrickel, J. W., Andrié, R. P., (2017). Relaxin reduces susceptibility to post-infarct atrial fibrillation in mice due to anti-fibrotic and anti-inflammatory properties Biochemical and Biophysical Research Communications 490, (3), 643-649

Background Relaxin-2 (RLX) is a peptide hormone that exerts beneficial anti-fibrotic and anti-inflammatory effects in diverse models of cardiovascular disease. The goal of this study was to determine the effects of RLX treatment on the susceptibility to atrial fibrillation (AF) after myocardial infarction (MI). Methods Mice with cryoinfarction of the left anterior ventricular wall were treated for two weeks with either RLX (75

Keywords: Atrial fibrillation, Atrial fibrosis, Myocardial infarction, Relaxin-2

Perea-Gil, I., Uriarte, J. J., Prat-Vidal, C., Gálvez-Montón, C., Roura, S., Llucià-Valldeperas, A., Soler-Botija, C., Farré, R., Navajas, D., Bayes-Genis, A., (2015). In vitro comparative study of two decellularization protocols in search of an optimal myocardial scaffold for recellularization American Journal of Translational Research 7, (3), 558-573

Introduction. Selection of a biomaterial-based scaffold that mimics native myocardial extracellular matrix (ECM) architecture can facilitate functional cell attachment and differentiation. Although decellularized myocardial ECM accomplishes these premises, decellularization processes may variably distort or degrade ECM structure. Materials and methods. Two decellularization protocols (DP) were tested on porcine heart samples (epicardium, mid myocardium and endocardium). One protocol, DP1, was detergent-based (SDS and Triton X-100), followed by DNase I treatment. The other protocol, DP2, was focused in trypsin and acid with Triton X-100 treatments. Decellularized myocardial scaffolds were reseeded by embedding them in RAD16-I peptidic hydrogel with adipose tissue-derived progenitor cells (ATDPCs). Results. Both protocols yielded acellular myocardial scaffolds (~82% and ~94% DNA reduction for DP1 and DP2, respectively). Ultramicroscopic assessment of scaffolds was similar for both protocols and showed filamentous ECM with preserved fiber disposition and structure. DP1 resulted in more biodegradable scaffolds (P = 0.04). Atomic force microscopy revealed no substantial ECM stiffness changes post-decellularization compared to native tissue. The Young’s modulus did not differ between heart layers (P = 0.69) or decellularization protocols (P = 0.15). After one week, recellularized DP1 scaffolds contained higher cell density (236 ± 106 and 98 ± 56 cells/mm2 for recellularized DP1 and DP2 scaffolds, respectively; P = 0.04). ATDPCs in both DP1 and DP2 scaffolds expressed the endothelial marker isolectin B4, but only in the DP1 scaffold ATDPCs expressed the cardiac markers GATA4, connexin43 and cardiac troponin T. Conclusions. In our hands, DP1 produced myocardial scaffolds with higher cell repopulation and promotes ATDPCs expression of endothelial and cardiomyogenic markers.

Keywords: Acellular myocardial scaffold, Adipose tissue-derived progenitor cells, Decellularization protocols, Extracellular matrix, Myocardial infarction, Recellularization