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Basic Research in Cardiology

Jing Zhao, Jin-Lai Gao, Jun-Xue Zhu, Hai-Bin Zhu, Xuan Peng, Man Jiang, Yao Fu, Juan Xu, Xi-Hai Mao, Nan Hu, Ming-Hui Ma, De-Li Dong
Cardiomyocyte loss and cardiac fibrosis are the main characteristics of cardiac ischemia and heart failure, and mitochondrial function of cardiomyocytes is impaired in cardiac ischemia and heart failure, so the aim of this study is to identify fate variability of cardiomyocytes and cardiac fibroblasts with mitochondria inhibition and explore the underlying mechanism. The mitochondrial respiratory function was measured by using Oxygraph-2k high-resolution respirometry. The STAT3 expression and activity were evaluated by western blot...
February 14, 2019: Basic Research in Cardiology
Lisa Kraft, Tugs Erdenesukh, Martina Sauter, Carsten Tschöpe, Karin Klingel
Coxsackieviruses of group B (CVB) are well-known causes of acute and chronic myocarditis. Chronic myocarditis can evolve into dilated cardiomyopathy (DCM) characterized by fibrosis and cardiac remodeling. Interleukin-1β (IL-1β) plays a decisive role in the induction of the inflammatory response as a consequence of viral replication. In this study, we analyzed the effects of IL-1β neutralization on the transition of acute to chronic myocarditis in a mouse model of CVB3 myocarditis. Mice were treated with an anti-murine IL-1β antibody as a surrogate for Canakinumab at different time points post CVB3 infection...
January 23, 2019: Basic Research in Cardiology
Fábio Trindade, Rui Vitorino, Adelino Leite-Moreira, Inês Falcão-Pires
The remote but heart-encircling location of pericardial fluid confers this biofluid unique properties. Once past the limitation of the invasive collection, for instance, on occasion of heart surgery or pericardiocentesis, the scrutiny of pericardial fluid content can be of great interest in cardiovascular research. This liquid concentrates many heart-derived factors, thus enclosing several surrogate markers for the diagnosis or prognosis of a large spectrum of diseases either pericardial (e.g. malignant or tuberculous pericarditis) or non-pericardial/heart diseases (e...
January 18, 2019: Basic Research in Cardiology
David J Polhemus, Rishi K Trivedi, Thomas E Sharp, Zhen Li, Traci T Goodchild, Amy Scarborough, Geoffrey de Couto, Eduardo Marbán, David J Lefer
Enthusiasm for cell therapy for myocardial injury has waned due to equivocal benefits in clinical trials. In an attempt to improve efficacy, we investigated repeated cell therapy and adjunct renal denervation (RDN) as strategies for augmenting cardioprotection with cardiosphere-derived cells (CDCs). We hypothesized that combining CDC post-conditioning with repeated CDC doses or delayed RDN therapy would result in superior function and remodeling. Wistar-Kyoto (WKY) rats or spontaneously hypertensive rats (SHR) were subjected to 45 min of coronary artery ligation followed by reperfusion for 12-14 weeks...
January 17, 2019: Basic Research in Cardiology
Swenja Kröller-Schön, Thomas Jansen, Thi Lan P Tran, Miroslawa Kvandová, Sanela Kalinovic, Matthias Oelze, John F Keaney, Marc Foretz, Benoit Viollet, Andreas Daiber, Sabine Kossmann, Jeremy Lagrange, Katie Frenis, Philip Wenzel, Thomas Münzel, Eberhard Schulz
Mice with a global deletion of α1AMPK are characterized by endothelial dysfunction and NADPH oxidase subunit 2 (NOX-2)-mediated vascular oxidative stress. However, the underlying mechanisms are incompletely understood and may involve endothelial NOX-2 upregulation or facilitated vascular infiltration of phagocytic cells. Therefore, the current study was designed to investigate the vascular effects of chronic angiotensin II (AngII) infusion in mice with an endothelial-specific α1AMPK deletion. A mouse strain with endothelial-specific α1AMPK deletion was generated by breeding α1AMPKflox/flox mice with TekCre+ or Cadh5Cre+ mice...
January 14, 2019: Basic Research in Cardiology
Tarja Alakoski, Johanna Ulvila, Raisa Yrjölä, Laura Vainio, Johanna Magga, Zoltan Szabo, Jonathan D Licht, Risto Kerkelä
Sprouty1 (Spry1) is a negative modulator of receptor tyrosine kinase signaling, but its role in cardiomyocyte survival has not been elucidated. The aim of this study was to investigate the potential role of cardiomyocyte Spry1 in cardiac ischemia-reperfusion (I/R) injury. Infarct areas of mouse hearts showed an increase in Spry1 protein expression, which localized to cardiomyocytes. To investigate if cardiomyocyte Spry1 regulates I/R injury, 8-week-old inducible cardiomyocyte Spry1 knockout (Spry1 cKO) mice and control mice were subjected to cardiac I/R injury...
January 11, 2019: Basic Research in Cardiology
Alan J Mouton, Yonggang Ma, Osvaldo J Rivera Gonzalez, Michael J Daseke, Elizabeth R Flynn, Tom C Freeman, Michael R Garrett, Kristine Y DeLeon-Pennell, Merry L Lindsey
Cardiac fibroblasts are the major producers of extracellular matrix (ECM) to form infarct scar. We hypothesized that fibroblasts undergo a spectrum of phenotype states over the course of myocardial infarction (MI) from early onset to scar formation. Fibroblasts were isolated from the infarct region of C57BL/6J male mice (3-6 months old, n = 60) at days 0 (no MI control) and 1, 3, or 7 after MI. Whole transcriptome analysis was performed by RNA-sequencing. Of the genes sequenced, 3371 were differentially expressed after MI...
January 11, 2019: Basic Research in Cardiology
Ines Garcia-Lunar, Daniel Pereda, Evelyn Santiago, Nuria Solanes, Jorge Nuche, María Ascaso, Joaquim Bobí, Federico Sierra, Ana Paula Dantas, Carlos Galán, Rodolfo San Antonio, Damián Sánchez-Quintana, Javier Sánchez-González, Joan Albert Barberá, Montserrat Rigol, Valentín Fuster, Borja Ibáñez, Manel Sabaté, Ana García-Álvarez
There is scarce evidence for pulmonary artery denervation (PADN) as a potential treatment for chronic postcapillary pulmonary hypertension (PH). We aimed to perform a proof-of-concept of PADN in a translational model of chronic PH. Nineteen pigs with chronic postcapillary PH (secondary to pulmonary vein banding) were randomized to surgical-PADN (using bipolar radiofrequency clamps) or sham procedure. Additionally, 6 healthy animals underwent percutaneous-PADN to compare the pulmonary artery (PA) lesion generated with both approaches...
January 11, 2019: Basic Research in Cardiology
Mira Jung, Michael Dodsworth, Thomas Thum
Myocardial infarction triggers infiltration of several types of immune cells that coordinate both innate and adaptive immune responses. These play a dual role in post-infarction cardiac remodeling by initiating and resolving inflammatory processes, which needs to occur in a timely and well-orchestrated way to ensure a reestablishment of normalized cardiac functions. Thus, therapeutic modulation of immune responses might have benefits for infarct patients. While such strategies have shown great potential in treating cancer, applications in the post-infarction context have been disappointing...
December 6, 2018: Basic Research in Cardiology
Joseph B Moore, Xian-Liang Tang, John Zhao, Annalara G Fischer, Wen-Jian Wu, Shizuka Uchida, Anna M Gumpert, Heather Stowers, Marcin Wysoczynski, Roberto Bolli
Preclinical investigations support the concept that donor cells more oriented towards a cardiovascular phenotype favor repair. In light of this philosophy, we previously identified HDAC1 as a mediator of cardiac mesenchymal cell (CMC) cardiomyogenic lineage commitment and paracrine signaling potency in vitro-suggesting HDAC1 as a potential therapeutically exploitable target to enhance CMC cardiac reparative capacity. In the current study, we examined the effects of pharmacologic HDAC1 inhibition, using the benzamide class 1 isoform-selective HDAC inhibitor entinostat (MS-275), on CMC cardiomyogenic lineage commitment and CMC-mediated myocardial repair in vivo...
November 16, 2018: Basic Research in Cardiology
Christian Riehle, Johann Bauersachs
Diabetes mellitus increases the risk of heart failure independent of co-existing hypertension and coronary artery disease. Although several molecular mechanisms for the development of diabetic cardiomyopathy have been identified, they are incompletely understood. The pathomechanisms are multifactorial and as a consequence, no causative treatment exists at this time to modulate or reverse the molecular changes contributing to accelerated cardiac dysfunction in diabetic patients. Numerous animal models have been generated, which serve as powerful tools to study the impact of type 1 and type 2 diabetes on the heart...
November 15, 2018: Basic Research in Cardiology
Ellis N Ter Horst, Paul A J Krijnen, Nazanin Hakimzadeh, Lourens F H J Robbers, Alexander Hirsch, Robin Nijveldt, Ingrid Lommerse, Ruud D Fontijn, Elisa Meinster, Ronak Delewi, Niels van Royen, Felix Zijlstra, Albert C van Rossum, C Ellen van der Schoot, Tineke C T M van der Pouw Kraan, Anton J Horrevoets, Anja M van der Laan, Hans W M Niessen, Jan J Piek
Monocytes are involved in adverse left ventricular (LV) remodelling following myocardial infarction (MI). To provide therapeutic opportunities we aimed to identify gene transcripts in monocytes that relate to post-MI healing and evaluated intervention with the observed gene activity in a rat MI model. In 51 MI patients treated by primary percutaneous coronary intervention (PCI), the change in LV end-diastolic volume index (EDVi) from baseline to 4-month follow-up was assessed using cardiovascular magnetic resonance imaging (CMR)...
November 12, 2018: Basic Research in Cardiology
Kristin S Edwards, Sadia Ashraf, Tyler M Lomax, Jessica M Wiseman, Michael E Hall, Fabio N Gava, John E Hall, Jonathan P Hosler, Romain Harmancey
Patients with insulin resistance and type 2 diabetes have poor cardiac outcomes following myocardial infarction (MI). The mitochondrial uncoupling protein 3 (UCP3) is down-regulated in the heart with insulin resistance. We hypothesized that decreased UCP3 levels contribute to poor cardiac recovery following ischemia/reperfusion (I/R). After confirming that myocardial UCP3 levels were systematically decreased by 20-49% in animal models of insulin resistance and type 2 diabetes, we genetically engineered Sprague-Dawley rats with partial loss of UCP3 (ucp3+/- )...
October 29, 2018: Basic Research in Cardiology
Parul Mehra, Yiru Guo, Yibing Nong, Pawel Lorkiewicz, Marjan Nasr, Qianhong Li, Senthilkumar Muthusamy, James A Bradley, Aruni Bhatnagar, Marcin Wysoczynski, Roberto Bolli, Bradford G Hill
Although cell therapy improves cardiac function after myocardial infarction, highly variable results and limited understanding of the underlying mechanisms preclude its clinical translation. Because many heart failure patients are diabetic, we examined how diabetic conditions affect the characteristics of cardiac mesenchymal cells (CMC) and their ability to promote myocardial repair in mice. To examine how diabetes affects CMC function, we isolated CMCs from non-diabetic C57BL/6J (CMCWT ) or diabetic B6.BKS(D)-Leprdb/J (CMCdb/db ) mice...
October 23, 2018: Basic Research in Cardiology
Julian Merz, Philipp Albrecht, Sunaina von Garlen, Ibrahim Ahmed, Daniel Dimanski, Dennis Wolf, Ingo Hilgendorf, Carmen Härdtner, Katja Grotius, Florian Willecke, Timo Heidt, Heiko Bugger, Natalie Hoppe, Ulrich Kintscher, Constantin von Zur Mühlen, Marco Idzko, Christoph Bode, Andreas Zirlik, Peter Stachon
Sterile inflammation of visceral fat, provoked by dying adipocytes, links the metabolic syndrome to cardiovascular disease. Danger-associated molecular patterns, such as adenosine triphosphate (ATP), are released by activated or dying cells and orchestrate leukocyte infiltration and inflammation via the purinergic receptor P2Y2 . The gene expression of ATP receptor P2Y2 did not change in several tissues in the course of obesity, but was increased within epididymal fat. Adipose tissue from P2Y 2 -/- mice consuming high-fat diet (HFD) contained less crown-like structures with a reduced frequency of adipose tissue macrophages (ATMs)...
October 18, 2018: 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
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