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Basic Research in Cardiology

Ingmar Sören Meyer, Florian Leuschner
Various cell types are involved in the healing process after myocardial infarction (MI). Besides cardiac resident cells (such as cardiomyocytes, fibroblasts and endothelial cells) already present at the lesion site, a massive influx of leukocytes (mainly monocytes and neutrophils) is observed within hours after the ischemic event. So far, little is known about modes of interaction of these cells. Wnt signaling is an evolutionary conserved signaling cassette known to play an important role in cell-cell communication...
October 16, 2018: Basic Research in Cardiology
Sean M Davidson, Sapna Arjun, Maryna V Basalay, Robert M Bell, Daniel I Bromage, Hans Erik Bøtker, Richard D Carr, John Cunningham, Arjun K Ghosh, Gerd Heusch, Borja Ibanez, Petra Kleinbongard, Sandrine Lecour, Helen Maddock, Michel Ovize, Malcolm Walker, Marlene Wiart, Derek M Yellon
Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy...
October 11, 2018: Basic Research in Cardiology
Andrey Kazakov, Rabea A Hall, Christian Werner, Timo Meier, André Trouvain, Svetlana Rodionycheva, Alexander Nickel, Frank Lammert, Christoph Maack, Michael Böhm, Ulrich Laufs
Fibrosis is a hallmark of maladaptive cardiac remodelling. Here we report that genome-wide quantitative trait locus (QTL) analyses in recombinant inbred mouse lines of C57BL/6 J and DBA2/J strains identified Raf Kinase Inhibitor Protein (RKIP) as genetic marker of fibrosis progression. C57BL/6 N-RKIP-/- mice demonstrated diminished fibrosis induced by transverse aortic constriction (TAC) or CCl4 (carbon tetrachloride) treatment compared with wild-type controls. TAC-induced expression of collagen Iα2 mRNA, Ki67+ fibroblasts and marker of oxidative stress 8-hydroxyguanosine (8-dOHG)+ fibroblasts as well as the number of fibrocytes in the peripheral blood and bone marrow were markedly reduced in C57BL/6 N-RKIP-/- mice...
September 6, 2018: Basic Research in Cardiology
Julia Krause, Alexandra Löser, Marc D Lemoine, Torsten Christ, Katharina Scherschel, Christian Meyer, Stefan Blankenberg, Tanja Zeller, Thomas Eschenhagen, Justus Stenzig
Engineered heart tissue (EHT) from rat cells is a useful tool to study ventricular biology and cardiac drug safety. Since atrial and ventricular cells differ significantly, EHT and other 3D cell culture formats generated from ventricular cells have been of limited value to study atrial biology. To date, reliable in vitro models that reflect atrial physiology are lacking. Therefore, we established a novel EHT model using rat atrial cells (atrial EHT, aEHT) to assess atrial physiology, contractility and drug response...
September 3, 2018: Basic Research in Cardiology
Kristine Y DeLeon-Pennell, Alan J Mouton, Osasere K Ero, Yonggang Ma, Rugmani Padmanabhan Iyer, Elizabeth R Flynn, Ingrid Espinoza, Solomon K Musani, Ramachandran S Vasan, Michael E Hall, Ervin R Fox, Merry L Lindsey
Sex differences in heart failure development following myocardial infarction (MI) are not fully understood. We hypothesized that differential MI signaling could explain variations in outcomes. Analysis of the mouse heart attack research tool 1.0 (422 mice; young = 5.4 ± 0.1; old = 23.3 ± 0.1 months of age) was used to dissect MI signaling pathways, which was validated in a new cohort of mice (4.8 ± 0.2 months of age); and substantiated in humans. Plasma collected at visit 2 from the MI subset of the Jackson Heart Study (JHS; a community-based study consisting of middle aged and older adults of African ancestry) underwent glycoproteomics grouped by outcome: (1) heart failure hospitalization after visit 2 (n = 3 men/12 women) and (2) without hospitalization through 2012 (n = 24 men/21 women)...
August 21, 2018: Basic Research in Cardiology
Hans Erik Bøtker, Derek Hausenloy, Ioanna Andreadou, Salvatore Antonucci, Kerstin Boengler, Sean M Davidson, Soni Deshwal, Yvan Devaux, Fabio Di Lisa, Moises Di Sante, Panagiotis Efentakis, Saveria Femminò, David García-Dorado, Zoltán Giricz, Borja Ibanez, Efstathios Iliodromitis, Nina Kaludercic, Petra Kleinbongard, Markus Neuhäuser, Michel Ovize, Pasquale Pagliaro, Michael Rahbek-Schmidt, Marisol Ruiz-Meana, Klaus-Dieter Schlüter, Rainer Schulz, Andreas Skyschally, Catherine Wilder, Derek M Yellon, Peter Ferdinandy, Gerd Heusch
No abstract text is available yet for this article.
August 17, 2018: Basic Research in Cardiology
Edward D Coverstone, Richard G Bach, LiShiun Chen, Laura J Bierut, Allie Y Li, Petra A Lenzini, Heidi C O'Neill, John A Spertus, Carmen C Sucharov, Jerry A Stitzel, Joel D Schilling, Sharon Cresci
The CHRNA5 gene encodes a neurotransmitter receptor subunit involved in multiple processes, including cholinergic autonomic nerve activity and inflammation. Common variants in CHRNA5 have been linked with atherosclerotic cardiovascular disease. Association of variation in CHRNA5 and specific haplotypes with cardiovascular outcomes has not been described. The aim of this study was to examine the association of CHRNA5 haplotypes with gene expression and mortality among patients with acute myocardial infarction (AMI) and explore potential mechanisms of this association...
August 10, 2018: Basic Research in Cardiology
Heng Zhou, Ning Li, Yuan Yuan, Ya-Ge Jin, Haipeng Guo, Wei Deng, Qi-Zhu Tang
Cardiovascular diseases (CVDs) are the primary causes of death worldwide. Among the numerous signaling molecules involved in CVDs, transcriptional factors directly influence gene expression and play a critical role in regulating cell function and the development of diseases. Activating transcription factor (ATF) 3 is an adaptive-response gene in the ATF/cAMP responsive element-binding (CREB) protein family of transcription factors that acts as either a repressor or an activator of transcription via the formation of homodimers or heterodimers with other ATF/CREB members...
August 9, 2018: Basic Research in Cardiology
Jing Li, Sean XiaoXiao Cai, Quan He, Helena Zhang, Daniel Friedberg, Fangfei Wang, Andrew N Redington
MicroRNA-144 is a cytoprotective miRNA. Our previous study showed that miR-144 provides potent acute cardioprotection in an ischemia/reperfusion injury model. This study was performed to further assess whether miR-144 improves post-MI remodeling in a non-reperfused myocardial infarction (MI) model. C57BL/6 mice were subjected to MI by permanent left anterior descending artery (LAD) ligation. miR-144 was delivered by intravenous injections of 8 mg/kg, 16 mg/kg, or 32 mg/kg at day 0, day 1, day 3, and then a similar dose given once every 3 days, until day 28 after MI...
August 6, 2018: Basic Research in Cardiology
Yonis Abukar, Rohit Ramchandra, Sally G Hood, Michael J McKinley, Lindsea C Booth, Song T Yao, Clive N May
Increased cardiac sympathetic nerve activity (CSNA) is a key feature of heart failure (HF) and is associated with poor outcome. There is evidence that central angiotensinergic mechanisms contribute to the increased CSNA in HF, but the central sites involved are unknown. In an ovine, rapid pacing model of HF, we investigated the contribution of the lamina terminalis and area postrema to the increased CSNA and also the responses to fourth ventricular infusion of the angiotensin type 1 receptor antagonist losartan...
August 3, 2018: Basic Research in Cardiology
Andreas Deussen
No abstract text is available yet for this article.
August 3, 2018: Basic Research in Cardiology
Alexander M Kiel, Adam G Goodwill, Hana E Baker, Gregory M Dick, Johnathan D Tune
The local metabolic hypothesis proposes that myocardial oxygen tension determines the degree of autoregulation by increasing the production of vasodilator metabolites as perfusion pressure is reduced. Thus, normal physiologic levels of coronary venous PO2 , an index of myocardial oxygenation, are proposed to be required for effective autoregulation. The present study challenged this hypothesis through determination of coronary responses to changes in coronary perfusion pressure (CPP 140-40 mmHg) in open-chest swine in the absence (n = 7) and presence of euvolemic hemodilution (~ 50% reduction in hematocrit), with (n = 5) and without (n = 6) infusion of dobutamine to augment MVO2 ...
August 2, 2018: Basic Research in Cardiology
Jonathon P Audia, Xi-Ming Yang, Edward S Crockett, Nicole Housley, Ehtesham Ul Haq, Kristen O'Donnell, Michael V Cohen, James M Downey, Diego F Alvarez
Patients with acute myocardial infarction receive a P2Y12 receptor antagonist prior to reperfusion, a treatment that has reduced, but not eliminated, mortality, or heart failure. We tested whether the caspase-1 inhibitor VX-765 given at reperfusion (a requirement for clinical use) can provide sustained reduction of infarction and long-term preservation of ventricular function in a pre-clinical model of ischemia/reperfusion that had been treated with a P2Y12 receptor antagonist. To address, the hypothesis open-chest rats were subjected to 60-min left coronary artery branch occlusion/120-min reperfusion...
July 10, 2018: Basic Research in Cardiology
Franz Hofmann
The underlying cause of cardiac hypertrophy, fibrosis, and heart failure has been investigated in great detail using different mouse models. These studies indicated that cGMP and cGMP-dependent protein kinase type I (cGKI) may ameliorate these negative phenotypes in the adult heart. Recently, evidence has been published that cardiac mitochondrial BKCa channels are a target for cGKI and that activation of mitoBKCa channels may cause some of the positive effects of conditioning in ischemia/reperfusion injury...
June 22, 2018: Basic Research in Cardiology
C Gebhard, F Maafi, B E Stähli, J Dang, W Nachar, A B de Oliveira Moraes, A E Kernaleguen, V Lavoie, M Mecteau, T Mihalache-Avram, Y Shi, M Chabot-Blanchet, D Busseuil, D Rhainds, E Rhéaume, Jean-Claude Tardif
Aortic valve stenosis (AVS) is the most common valvular heart disease in the Western world. Therapy based on apolipoprotein A-I (apoA-I), the major protein component of high-density lipoproteins, results in AVS regression in experimental models. Nevertheless, apoA-I degradation by proteases might lead to suboptimal efficacy of such therapy. An activatable probe using a quenched fluorescently labeled full-length apoA-I protein was generated to assess apoA-I-degrading protease activity in plasma derived from 44 men and 20 women with severe AVS (age 65...
June 18, 2018: Basic Research in Cardiology
Jan Beckendorf, Maarten M G van den Hoogenhof, Johannes Backs
In the cardiomyocyte, CaMKII has been identified as a nodal influencer of excitation-contraction and also excitation-transcription coupling. Its activity can be regulated in response to changes in intracellular calcium content as well as after several post-translational modifications. Some of the effects mediated by CaMKII may be considered adaptive, while effects of sustained CaMKII activity may turn into the opposite and are detrimental to cardiac integrity and function. As such, CaMKII has long been noted as a promising target for pharmacological inhibition, but the ubiquitous nature of CaMKII has made it difficult to target CaMKII specifically where it is detrimental...
June 15, 2018: Basic Research in Cardiology
Lei Hou, Junjie Guo, Feng Xu, Xinyu Weng, Wenhui Yue, Junbo Ge
Asymmetric dimethylarginine (ADMA) is a risk factor for heart diseases. Dimethylarginine dimethylaminohydrolase (DDAH) enzymes are key proteins for ADMA degradation. Endothelial DDAH1 is a vital regulator of angiogenesis. DDAH1 is also expressed in cardiomyocytes. However, the role of DDAH1 in cardiomyocytes needs further clarification. Herein, we used an inducible cardiac-specific DDAH1 knockdown mouse (cardiac DDAH1-/- ) to investigate the role of cardiomyocyte DDAH1 in left-ventricular (LV) remodeling after acute myocardial infarction (AMI)...
June 11, 2018: Basic Research in Cardiology
Felix Wiedmann, Jan S Schulte, Bruna Gomes, Maria-Patapia Zafeiriou, Antonius Ratte, Franziska Rathjens, Edda Fehrmann, Beatrix Scholz, Niels Voigt, Frank Ulrich Müller, Dierk Thomas, Hugo A Katus, Constanze Schmidt
Understanding molecular mechanisms involved in atrial tissue remodeling and arrhythmogenesis in atrial fibrillation (AF) is essential for developing specific therapeutic approaches. Two-pore-domain potassium (K2P ) channels modulate cellular excitability, and TASK-1 (K2P 3.1) currents were recently shown to alter atrial action potential duration in AF and heart failure (HF). Finding animal models of AF that closely resemble pathophysiological alterations in human is a challenging task. This study aimed to analyze murine cardiac expression patterns of K2P channels and to assess modulation of K2P channel expression in murine models of AF and HF...
June 7, 2018: Basic Research in Cardiology
Alan J Mouton, Kristine Y DeLeon-Pennell, Osvaldo J Rivera Gonzalez, Elizabeth R Flynn, Tom C Freeman, Jeffrey J Saucerman, Michael R Garrett, Yonggang Ma, Romain Harmancey, Merry L Lindsey
In response to myocardial infarction (MI), cardiac macrophages regulate inflammation and scar formation. We hypothesized that macrophages undergo polarization state changes over the MI time course and assessed macrophage polarization transcriptomic signatures over the first week of MI. C57BL/6 J male mice (3-6 months old) were subjected to permanent coronary artery ligation to induce MI, and macrophages were isolated from the infarct region at days 1, 3, and 7 post-MI. Day 0, no MI resident cardiac macrophages served as the negative MI control...
June 4, 2018: Basic Research in Cardiology
Marina V Basalay, Sean M Davidson, Andrey V Gourine, Derek M Yellon
Remote ischaemic conditioning (RIC) is a promising method of cardioprotection, with numerous clinical studies having demonstrated its ability to reduce myocardial infarct size and improve prognosis. On the other hand, there are several clinical trials, in particular those conducted in the setting of elective cardiac surgery, that have failed to show any benefit of RIC. These contradictory data indicate that there is insufficient understanding of the mechanisms underlying RIC. RIC is now known to signal indiscriminately, protecting not only the heart, but also other organs...
June 1, 2018: Basic Research in Cardiology
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