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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
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
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