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Basic Research in Cardiology

Hector A Cabrera-Fuentes, Julian Aragones, Jürgen Bernhagen, Andreas Boening, William A Boisvert, Hans E Bøtker, Heerajnarain Bulluck, Stuart Cook, Fabio Di Lisa, Felix B Engel, Bernd Engelmann, Fulvia Ferrazzi, Péter Ferdinandy, Alan Fong, Ingrid Fleming, Erich Gnaiger, Sauri Hernández-Reséndiz, Siavash Beikoghli Kalkhoran, Moo Hyun Kim, Sandrine Lecour, Elisa A Liehn, Michael S Marber, Manuel Mayr, Tetsuji Miura, Sang-Bing Ong, Karlheinz Peter, Daniel Sedding, Manvendra K Singh, M Saadeh Suleiman, Hans J Schnittler, Rainer Schulz, Winston Shim, Daniel Tello, Carl-Wilhelm Vogel, Malcolm Walker, Qilong Oscar Yang Li, Derek M Yellon, Derek J Hausenloy, Klaus T Preissner
In this meeting report, particularly addressing the topic of protection of the cardiovascular system from ischemia/reperfusion injury, highlights are presented that relate to conditioning strategies of the heart with respect to molecular mechanisms and outcome in patients' cohorts, the influence of co-morbidities and medications, as well as the contribution of innate immune reactions in cardioprotection. Moreover, developmental or systems biology approaches bear great potential in systematically uncovering unexpected components involved in ischemia-reperfusion injury or heart regeneration...
November 2016: Basic Research in Cardiology
Natalie Weber, Kristin Schwanke, Stephan Greten, Meike Wendland, Bogdan Iorga, Martin Fischer, Cornelia Geers-Knörr, Jan Hegermann, Christoph Wrede, Jan Fiedler, Henning Kempf, Annika Franke, Birgit Piep, Angelika Pfanne, Thomas Thum, Ulrich Martin, Bernhard Brenner, Robert Zweigerdt, Theresia Kraft
Human pluripotent stem cell (hPSC)-derived cardiomyocytes hold great potential for in vitro modeling of diseases like cardiomyopathies. Yet, knowledge about expression and functional impact of sarcomeric protein isoforms like the myosin heavy chain (MyHC) in hPSC-cardiomyocytes is scarce. We hypothesized that ventricular β-MyHC expression alters contraction and calcium kinetics and drives morphological and electrophysiological differentiation towards ventricular-like cardiomyocytes. To address this, we (1) generated human embryonic stem cell-derived cardiomyocytes (hESC-CMs) that switched towards exclusive β-MyHC, and (2) functionally and morphologically characterized these hESC-CMs at the single-cell level...
November 2016: Basic Research in Cardiology
M Borrell-Pages, G Vilahur, J C Romero, L Casaní, M T Bejar, L Badimon
LRP5 (low-density lipoprotein receptor-related protein 5) activates canonical Wnt signalling. LRP5 plays multiple roles including regulation of lipoprotein and cholesterol homeostasis as well as innate immunity cell function. However, it is not known whether LRP5 has a role in the myocardium. The aim of this study was to investigate LRP5 and Wnt signalling in myocardial remodelling after acute myocardial infarction (MI). Wnt protein levels were determined in a hypercholesterolemic porcine model of MI, in Lrp5 (-/-) C57Bl6 mice, in cultured cardiomyocytes and in human explanted hearts with previous MI episodes...
November 2016: Basic Research in Cardiology
Friederike Cuello, Kristina Lorenz
No abstract text is available yet for this article.
November 2016: Basic Research in Cardiology
Michael M Kreusser, Lorenz H Lehmann, Nora Wolf, Stanislav Keranov, Andreas Jungmann, Hermann-Josef Gröne, Oliver J Müller, Hugo A Katus, Johannes Backs
CaM kinase II (CaMKII) has been suggested to drive pathological cardiac remodeling and heart failure. However, the evidence provided so far is based on inhibitory strategies using chemical compounds and peptides that also exert off-target effects and followed exclusively preventive strategies. Therefore, the aim of this study was to investigate whether specific CaMKII inhibition after the onset of cardiac stress delays or reverses maladaptive cardiac remodeling and dysfunction. Combined genetic deletion of the two redundant CaMKII genes δ and γ was induced after the onset of overt heart failure as the result of pathological pressure overload induced by transverse aortic constriction (TAC)...
November 2016: Basic Research in Cardiology
Bernhard J Haubner, Thomas Schuetz, Josef M Penninger
Cardiac regeneration is one of the prime visions in cardiovascular research. The mouse neonatal apical resection and left anterior descending artery (LAD) ligation model introduced novel in vivo mammalian assays to study cardiac regeneration. However, recent reports and editorials discussed and critically questioned the value and technical reproducibility of the mouse neonatal myocardial infarction approach, making it paramount to develop and use a reproducible model system. We established a mouse neonatal myocardial infarction model by visually confirmed ligation of the LAD using microsurgery...
November 2016: Basic Research in Cardiology
Zewei Sun, Dongchen Zhou, Xudong Xie, Shuai Wang, Zhen Wang, Wenting Zhao, Hongfei Xu, Liangrong Zheng
Increased macrophage accumulation occurs in the atria of patients with atrial fibrillation (AF). However, the phenotype and functions of the macrophages in AF remain unclear. We investigated the macrophage-atrial myocyte interaction in AF patients and found that the increased macrophages were mainly pro-inflammatory macrophages (iNOS(+), Arg1(-)). Tachypacing of HL-1 atrial myocytes also led to pro-inflammatory macrophage polarization. In addition, lipopolysaccharide (LPS)-stimulated pro-inflammatory macrophages-induced atrial electrical remodeling, evidenced by increased AF incidence and decreased atrial effective refractory period and L-type calcium currents (I Ca-L) in both canine and mouse AF models...
November 2016: Basic Research in Cardiology
Yikui Tian, Dongfeng Pan, Mahendra D Chordia, Brent A French, Irving L Kron, Zequan Yang
The spleen plays a critical role in post-infarct myocardial remodeling. However, the role of the spleen in exacerbating myocardial infarction (MI) during acute ischemia/reperfusion (I/R) injury is unknown. The present study tests the hypothesis that splenic leukocytes are activated by substances released from ischemic myocardium to subsequently exacerbate myocardial injury during reperfusion. The left coronary artery in C57BL/6 mice underwent various durations of occlusion followed by 60 min of reperfusion (denoted as min/min of I/R) with or without splenectomy prior to I/R injury...
November 2016: Basic Research in Cardiology
Shawn B Bender, Vincent J de Beer, Darla L Tharp, Douglas K Bowles, M Harold Laughlin, Daphne Merkus, Dirk J Duncker
Accelerated development of coronary atherosclerosis is a defining characteristic of familial hypercholesterolemia (FH). However, the recent data highlight a significant cardiovascular risk prior to the development of critical coronary stenosis. We, therefore, examined the hypothesis that FH produces coronary microvascular dysfunction and impairs coronary vascular control at rest and during exercise in a swine model of FH. Coronary vascular responses to drug infusions and exercise were examined in chronically instrumented control and FH swine...
November 2016: Basic Research in Cardiology
Zarha Vermeulen, Vincent F M Segers, Gilles W De Keulenaer
The dual role of ErbB2 (or HER-2) in tumor growth and in physiological adaptive reactions of the heart positions ErbB2 at the intersection between cancer and chronic heart failure. Accordingly, ErbB2-targeted inhibitory therapy of cancer may lead to ventricular dysfunction, and activation of ErbB2 for heart failure therapy may induce malignancy. The molecular processes leading to the activation of ErbB2 in tumors and cardiac cells are, however, fundamentally different from each other. Thus, it must be feasible to design drugs that specifically target either physiological or malignant ErbB2 signaling, to activate ErbB2 signaling in heart failure with no increased risk for cancer, and to inhibit ErbB2 signaling in cancer with no increased risk for heart failure...
November 2016: Basic Research in Cardiology
Yi Dong, Vishnu V R Undyala, Karin Przyklenk
Recent attention has focused on the concept that mitochondrial dynamics-that is, the balance between mitochondrial fusion and fission (fragmentation)-may play a pivotal role in determining cell fate in the setting of myocardial ischemia-reperfusion injury. In this regard, there is an emerging consensus that: (1) ischemia-reperfusion favors mitochondrial fragmentation and (2) strategies aimed at inhibiting the translocation of dynamin-related protein 1 (DRP1: the 'master regulator' of fission) from the cytosol to the mitochondria, when initiated as a pretreatment, are cardioprotective...
September 2016: Basic Research in Cardiology
Yung-Hsin Yeh, Lung-An Hsu, Ying-Hwa Chen, Chi-Tai Kuo, Gwo-Jyh Chang, Wei-Jan Chen
Structural and electrical remodeling in the atrium constitutes the main feature of atrial fibrillation (AF), which is characterized by increased oxidative stress. Heme oxygenase-1 (HO-1) is a potent anti-oxidant system that may provide protection against various oxidative stress-related diseases. The aim of this study is to investigate whether HO-1 has a protective effect on AF-related remodeling. Cultured atrium-derived myocytes (HL-1 cell line) were used to evaluate tachypacing-induced oxidative stress, structural, and electrical remodeling...
September 2016: Basic Research in Cardiology
Wei Deng, Andrew R Ednie, Jianyong Qi, Eric S Bennett
Dilated cardiomyopathy (DCM), the third most common cause of heart failure, is often associated with arrhythmias and sudden cardiac death if not controlled. The majority of DCM is of unknown etiology. Protein sialylation is altered in human DCM, with responsible mechanisms not yet described. Here we sought to investigate the impact of clinically relevant changes in sialylation on cardiac function using a novel model for altered glycoprotein sialylation that leads to DCM and to chronic stress-induced heart failure (HF), deletion of the sialyltransferase, ST3Gal4...
September 2016: Basic Research in Cardiology
Adam G Goodwill, Jillian N Noblet, Daniel Sassoon, Lijuan Fu, Ghassan S Kassab, Luke Schepers, B Paul Herring, Trey S Rottgen, Johnathan D Tune, Gregory M Dick
Ion channels in smooth muscle control coronary vascular tone, but the identity of the potassium channels involved requires further investigation. The purpose of this study was to evaluate the functional role of KV1 channels on porcine coronary blood flow using the selective antagonist correolide. KV1 channel gene transcripts were found in porcine coronary arteries, with KCNA5 (encoding KV1.5) being most abundant (P < 0.001). Immunohistochemical staining demonstrated KV1.5 protein in the vascular smooth muscle layer of both porcine and human coronary arteries, including microvessels...
September 2016: Basic Research in Cardiology
Laetitia Vanhoutte, Bernhard L Gerber, Bernard Gallez, Chrystelle Po, Julie Magat, Jean-Luc Balligand, Olivier Feron, Stéphane Moniotte
No abstract text is available yet for this article.
September 2016: Basic Research in Cardiology
Alessandra Martire, Fikru B Bedada, Shizuka Uchida, Jochen Pöling, Marcus Krüger, Henning Warnecke, Manfred Richter, Thomas Kubin, Susanne Herold, Thomas Braun
Mesenchymal stem cells (MSC) have been used to treat different clinical conditions although the mechanisms by which pathogenetic processes are affected are still poorly understood. We have previously analyzed the homing of bone marrow-derived MSC to diseased tissues characterized by a high degree of mononuclear cell infiltration and postulated that MSC might modulate inflammatory responses. Here, we demonstrate that MSC mitigate adverse tissue remodeling, improve organ function, and extend lifespan in a mouse model of inflammatory dilative cardiomyopathy (DCM)...
September 2016: Basic Research in Cardiology
Sabine Ameling, Gourav Bhardwaj, Elke Hammer, Daniel Beug, Leif Steil, Yvonne Reinke, Kerstin Weitmann, Markus Grube, Christiane Trimpert, Karin Klingel, Reinhard Kandolf, Wolfgang Hoffmann, Matthias Nauck, Marcus Dörr, Klaus Empen, Stephan B Felix, Uwe Völker
Immunoadsorption with subsequent immunoglobulin substitution (IA/IgG) represents a therapeutic approach for patients with dilated cardiomyopathy (DCM). Here, we studied which molecular cardiac alterations are initiated after this treatment. Transcription profiling of endomyocardial biopsies with Affymetrix whole genome arrays was performed on 33 paired samples of DCM patients collected before and 6 months after IA/IgG. Therapy-related effects on myocardial protein levels were analysed by label-free proteome profiling for a subset of 23 DCM patients...
September 2016: Basic Research in Cardiology
Yuliya Mikhed, Jörg Fahrer, Matthias Oelze, Swenja Kröller-Schön, Sebastian Steven, Philipp Welschof, Elena Zinßius, Paul Stamm, Fatemeh Kashani, Siyer Roohani, Joana Melanie Kress, Elisabeth Ullmann, Lan P Tran, Eberhard Schulz, Bernd Epe, Bernd Kaina, Thomas Münzel, Andreas Daiber
Nitroglycerin (GTN) and other organic nitrates are widely used vasodilators. Their side effects are development of nitrate tolerance and endothelial dysfunction. Given the potential of GTN to induce nitro-oxidative stress, we investigated the interaction between nitro-oxidative DNA damage and vascular dysfunction in experimental nitrate tolerance. Cultured endothelial hybridoma cells (EA.hy 926) and Wistar rats were treated with GTN (ex vivo: 10-1000 µM; in vivo: 10, 20 and 50 mg/kg/day for 3 days, s.c...
July 2016: Basic Research in Cardiology
Jana Wobst, Simon von Ameln, Bernhard Wolf, Michael Wierer, Tan An Dang, Hendrik B Sager, Stephanie Tennstedt, Christian Hengstenberg, Doris Koesling, Andreas Friebe, Siegmund L Braun, Jeanette Erdmann, Heribert Schunkert, Thorsten Kessler
Stimulators of the soluble guanylyl cyclase (sGC) are emerging therapeutic agents in cardiovascular diseases. Genetic alterations of the GUCY1A3 gene, which encodes the α1 subunit of the sGC, are associated with coronary artery disease. Studies investigating sGC stimulators in subjects with CAD and carrying risk-related variants in sGC are, however, lacking. Here, we functionally investigate the impact of coding GUCY1A3 variants on sGC activity and the therapeutic potential of sGC stimulators in vitro. In addition to a known loss-of-function variant, eight coding variants in GUCY1A3 were cloned and expressed in HEK 293 cells...
July 2016: Basic Research in Cardiology
Jack M J Pickard, Sean M Davidson, Derek J Hausenloy, Derek M Yellon
The cardioprotection afforded by remote ischaemic conditioning (RIC) is mediated via a complex mechanism involving sensory afferent nerves, the vagus nerve, and release of a humoral blood-borne factor. However, it is unknown whether release of the protective factor depends on vagal activation or occurs independently. This study aimed to evaluate the co-dependence of the neural and humoral pathways of RIC, focussing on the vagus nerve and intrinsic cardiac ganglia. In the first study, anesthetised rats received bilateral cervical vagotomy or sham-surgery immediately prior to RIC (4 × 5 min limb ischemia-reperfusion) or sham-RIC...
July 2016: Basic Research in Cardiology
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