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Transverse aortic constriction

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https://www.readbyqxmd.com/read/28900153/genetic-ablation-of-fgf23-or-klotho-does-not-modulate-experimental-heart-hypertrophy-induced-by-pressure-overload
#1
Svetlana Slavic, Kristopher Ford, Magalie Modert, Amarela Becirovic, Stephan Handschuh, Andreas Baierl, Nejla Katica, Ute Zeitz, Reinhold G Erben, Olena Andrukhova
Left ventricular hypertrophy (LVH) ultimately leads to heart failure in conditions of increased cardiac pre- or afterload. The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Using transverse aortic constriction (TAC) in gene-targeted mouse models, we examine the role of Fgf23 and Klotho in cardiac hypertrophy and dysfunction induced by pressure overload. TAC profoundly increases serum intact Fgf23 due to increased cardiac and bony Fgf23 transcription and downregulation of Fgf23 cleavage...
September 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28874825/knockout-of-the-atpase-inhibitory-factor-1-protects-the-heart-from-pressure-overload-induced-cardiac-hypertrophy
#2
Kevin Yang, Qinqiang Long, Kamalamma Saja, Fengyuan Huang, Steven M Pogwizd, Lufang Zhou, Masasuke Yoshida, Qinglin Yang
Mitochondrial ATP synthase catalyzes the coupling of oxidative phosphorylation. Under pathological conditions, ATP synthase hydrolyzes ATP to replenish protons from the matrix into the intermembrane space, sustaining mitochondrial membrane potential. ATPase inhibitory factor 1 (IF1) is a nuclear-encoded, ATP synthase-interacting protein that selectively inhibits the hydrolysis activity of ATP synthase, which may render the protective role of IF1 in ischemic hearts. However, the in vivo cardiac function of IF1 and the potential therapeutic application targeting IF1 remain obscure...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28852941/monitoring-of-cardiac-remodeling-in-a-mouse-model-of-pressure-overload-left-ventricular-hypertrophy-with-18-f-fdg-micropet
#3
Andrei Todica, Nick L Beetz, Lisa Günther, Mathias J Zacherl, Ulrich Grabmaier, Bruno Huber, Peter Bartenstein, Stefan Brunner, Sebastian Lehner
PURPOSE: This study aims to analyze the left ventricular function parameters, scar load, and hypertrophy in a mouse model of pressure-overload left ventricular (LV) hypertrophy over the course of 8 weeks using 2-deoxy-2-[(18)F]fluoro-D-glucose ([(18)F]FDG) micro-positron emission tomography (microPET) imaging. PROCEDURES: LV hypertrophy was induced in C57BL/6 mice by transverse aortic constriction (TAC). Myocardial hypertrophy developed after 2-4 weeks. ECG-gated microPET scans with [(18)F]FDG were performed 4 and 8 weeks after surgery...
August 29, 2017: Molecular Imaging and Biology: MIB: the Official Publication of the Academy of Molecular Imaging
https://www.readbyqxmd.com/read/28835616/leukocytic-toll-like-receptor-2-deficiency-preserves-cardiac-function-and-reduces-fibrosis-in-sustained-pressure-overload
#4
Jiong-Wei Wang, Magda S C Fontes, Xiaoyuan Wang, Suet Yen Chong, Elise L Kessler, Ya-Nan Zhang, Judith J de Haan, Fatih Arslan, Saskia C A de Jager, Leo Timmers, Toon A B van Veen, Carolyn S P Lam, Dominique P V de Kleijn
An involement of Toll-like receptor 2 (TLR2) has been established in cardiac dysfunction after acute myocardial infarction; however, its role in chronic pressure overload is unclear. We sought to evaluate the role of TLR2 in cardiac hypertrophy, fibrosis and dysfunction in sustained pressure overload. We induced pressure overload via transverse aortic constriction (TAC) in TLR2(-/-) and wild type (WT) mice, and followed temporal changes over 8 weeks. Despite similar increases in heart weight, left ventricular (LV) ejection fraction (EF) and diastolic function (mitral E/A ratio) were preserved in TLR2(-/-) mice but impaired in WT mice following TAC...
August 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28827474/p2y12-receptor-promotes-pressure-overload-induced-cardiac-remodeling-via-platelet-driven-inflammation-in-mice
#5
Lujin Wu, Fujie Zhao, Meiyan Dai, Huaping Li, Chen Chen, Jiali Nie, Peihua Wang, Dao Wen Wang
Inflammation plays a critical role in adverse cardiac remodeling and heart failure. The P2y12 receptor is one of the predominant activating receptors for platelets, thus initiating inflammatory responses under various diseases. In this study, we investigated the functional significance of P2y12-mediated platelet activation in pressure overload-induced cardiac remodeling. Notably, P2y12 knockout (P2y12(-)(/-)) mice exhibited suppressed transverse aortic constriction-induced changes in cardiac hypertrophy, collagen synthesis, inflammatory cell recruitment, and cardiac dysfunction...
August 21, 2017: Hypertension
https://www.readbyqxmd.com/read/28822962/glucose-transporter-4-glut4-deficient-hearts-develop-maladaptive-hypertrophy-in-response-to-physiologic-or-pathologic-stresses
#6
Adam Raymond Wende, Jaetaek Kim, William Holland, Benjamin E Wayment, Brian T O'Neill, Joseph Tuinei, Manoja K Brahma, Mark E Pepin, Mark A McCrory, Ivan Luptak, Ganesh V Halade, Sheldon E Litwin, E Dale Abel
Pathological cardiac hypertrophy may be associated with reduced expression of the GLUT4 glucose transporter in contrast to exercise-induced cardiac hypertrophy, where GLUT4 levels are increased. However, mice with cardiac specific deletion of GLUT4 (G4H-/-) have normal cardiac function in the unstressed state. This study tested the hypothesis that cardiac GLUT4 is required for myocardial adaptations to hemodynamic demands. G4H-/- and control littermates (Con) were subjected to either a pathological model of left ventricular pressure overload (transverse aortic constriction; TAC) or a physiological model of endurance exercise (swim training)...
August 19, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28822689/cholesterol-lowering-gene-therapy-counteracts-the-development-of-non-ischemic-cardiomyopathy-in-mice
#7
Ilayaraja Muthuramu, Ruhul Amin, Andrey Postnov, Mudit Mishra, Joseph Pierre Aboumsallem, Tom Dresselaers, Uwe Himmelreich, Paul P Van Veldhoven, Olivier Gheysens, Frank Jacobs, Bart De Geest
A causal role of hypercholesterolemia in non-ischemic heart failure has never been demonstrated. Adeno-associated viral serotype 8 (AAV8)-low-density lipoprotein receptor (AAV8-LDLr) gene transfer was performed in LDLr-deficient mice without and with pressure overload induced by transverse aortic constriction (TAC). AAV8-LDLr gene therapy resulted in an 82.8% (p < 0.0001) reduction of plasma cholesterol compared with controls. Mortality rate was lower (p < 0.05) in AAV8-LDLr TAC mice compared with control TAC mice (hazard ratio for mortality 0...
August 1, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28820968/reduced-activin-receptor-like-kinase-1-activity-promotes-cardiac-fibrosis-in-heart-failure
#8
Kevin J Morine, Xiaoying Qiao, Vikram Paruchuri, Mark J Aronovitz, Emily E Mackey, Lyanne Buiten, Jonathan Levine, Keshan Ughreja, Prerna Nepali, Robert M Blanton, S Paul Oh, Richard H Karas, Navin K Kapur
INTRODUCTION: Activin receptor-like kinase 1 (ALK1) mediates signaling via the transforming growth factor beta-1 (TGFβ1), a pro-fibrogenic cytokine. No studies have defined a role for ALK1 in heart failure. HYPOTHESIS: We tested the hypothesis that reduced ALK1 expression promotes maladaptive cardiac remodeling in heart failure. METHODS AND RESULTS: In patients with advanced heart failure referred for left ventricular (LV) assist device implantation, LV Alk1 mRNA and protein levels were lower than control LV obtained from patients without heart failure...
July 18, 2017: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
https://www.readbyqxmd.com/read/28819685/cardiomyocyte-dimethylarginine-dimethylaminohydrolase-1-ddah1-plays-an-important-role-in-attenuating-ventricular-hypertrophy-and-dysfunction
#9
Xin Xu, Ping Zhang, Dongmin Kwak, John Fassett, Wenhui Yue, Dorothee Atzler, Xinli Hu, Xiaohong Liu, Huan Wang, Zhongbing Lu, Haipeng Guo, Edzard Schwedhelm, Rainer H Böger, Peijie Chen, Yingjie Chen
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability. Dimethylarginine dimethylaminohydrolase-1 (DDAH1) exerts a critical role for ADMA degradation and plays an important role in NO signaling. In the heart, DDAH1 is observed in endothelial cells and in the sarcolemma of cardiomyocytes. While NO signaling is important for cardiac adaptation to stress, DDAH1 impact on cardiomyocyte homeostasis is not clear. Here we used the MerCreMer-LoxP model to specifically disrupt cardiomyocyte DDAH1 expression in adult mice to determine the physiological impact of cardiomyocyte DDAH1 under basal conditions and during hypertrophic stress imposed by transverse aortic constriction (TAC)...
August 17, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28805231/the-histone-methyltransferase-mixed-lineage-leukemia-mll-3-may-play-a-potential-role-on-clinical-dilated-cardiomyopathy
#10
Ding-Sheng Jiang, Xin Yi, Rui Li, Yun-Shu Su, Jing Wang, Min-Lai Chen, Li-Gang Liu, Min Hu, Cai Cheng, Ping Zheng, Xue-Hai Zhu, Xiang Wei
Histone modifications play a critical role in the pathological processes of dilated cardiomyopathy (DCM). While the role and expression pattern of histone methyltransferases (HMTs), especially mixed lineage leukemia (MLL) families on DCM are unclear. To this end, twelve normal and fifteen DCM heart samples were included in the present study. A murine cardiac remodelling model was induced by transverse aortic constriction (TAC). Real-time PCR was performed to detect the expression levels of MLL families in the mouse and human left ventricles...
August 9, 2017: Molecular Medicine
https://www.readbyqxmd.com/read/28799247/the-valosin-containing-protein-is-a-novel-repressor-of-cardiomyocyte-hypertrophy-induced-by-pressure-overload
#11
Ning Zhou, Ben Ma, Shaunrick Stoll, Tristan T Hays, Hongyu Qiu
Hypertension-induced left ventricular hypertrophy (LVH) is an independent risk factor for heart failure. Regression of LVH has emerged as a major goal in the treatment of hypertensive patients. Here, we tested our hypothesis that the valosin-containing protein (VCP), an ATPase associate protein, is a novel repressor of cardiomyocyte hypertrophy under the pressure overload stress. Left ventricular hypertrophy (LVH) was determined by echocardiography in 4-month male spontaneously hypertensive rats (SHRs) vs. age-matched normotensive Wistar Kyoto (WKY) rats...
October 2017: Aging Cell
https://www.readbyqxmd.com/read/28790356/trpc6-counteracts-trpc3-nox2-protein-complex-leading-to-attenuation-of-hyperglycemia-induced-heart-failure-in-mice
#12
Sayaka Oda, Takuro Numaga-Tomita, Naoyuki Kitajima, Takashi Toyama, Eri Harada, Tsukasa Shimauchi, Akiyuki Nishimura, Tatsuya Ishikawa, Yoshito Kumagai, Lutz Birnbaumer, Motohiro Nishida
Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure...
August 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28759817/left-atrial-remodeling-hypertrophy-and-fibrosis-in-mouse-models-of-heart-failure
#13
Waqas Hanif, Linda Alex, Ya Su, Arti V Shinde, Ilaria Russo, Na Li, Nikolaos G Frangogiannis
Left ventricular dysfunction increases left atrial pressures and causes atrial remodeling. In human subjects, increased left atrial size is a powerful predictor of mortality and adverse events in a broad range of cardiac pathologic conditions. Moreover, structural remodeling of the atrium plays an important role in the pathogenesis of atrial tachyarrhythmias. Despite the potential value of the atrium in assessment of functional endpoints in myocardial disease, atrial pathologic alterations in mouse models of left ventricular disease have not been systematically investigated...
September 2017: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
https://www.readbyqxmd.com/read/28759639/g-protein-coupled-receptor-kinase-2-promotes-cardiac-hypertrophy
#14
Philipp Schlegel, Julia Reinkober, Eric Meinhardt, Henrike Tscheschner, Erhe Gao, Sarah M Schumacher, Ancai Yuan, Johannes Backs, Patrick Most, Thomas Wieland, Walter J Koch, Hugo A Katus, Philip W Raake
The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GRK2) is a hallmark of cardiac stress and heart failure. Inhibition of GRK2 improved cardiac function and survival and diminished cardiac remodeling in various animal heart failure models. The aim of the present study was to investigate the effects of GRK2 on cardiac hypertrophy and dissect potential molecular mechanisms. In mice we observed increased GRK2 mRNA and protein levels following transverse aortic constriction (TAC)...
2017: PloS One
https://www.readbyqxmd.com/read/28751527/in-utero-exposure-to-diesel-exhaust-particulates-is-associated-with-an-altered-cardiac-transcriptional-response-to-transverse-aortic-constriction-and-altered-dna-methylation
#15
Jamie M Goodson, Chad S Weldy, James W MacDonald, Yonggang Liu, Theo K Bammler, Wei-Ming Chien, Michael T Chin
In utero exposure to diesel exhaust air pollution has been associated with increased adult susceptibility to heart failure in mice, but the mechanisms by which this exposure promotes susceptibility to heart failure are poorly understood. To identify the potential transcriptional effects that mediate this susceptibility, we have performed RNA sequencing analysis on adult hearts from mice that were exposed to diesel exhaust in utero and that have subsequently undergone transverse aortic constriction. We identified 3 target genes, Mir133a-2, Ptprf, and Pamr1, which demonstrate dysregulation after exposure and aortic constriction...
July 27, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28718833/coconut-oil-aggravates-pressure-overload-induced-cardiomyopathy-without-inducing-obesity-systemic-insulin-resistance-or-cardiac-steatosis
#16
Ilayaraja Muthuramu, Ruhul Amin, Andrey Postnov, Mudit Mishra, Frank Jacobs, Olivier Gheysens, Paul P Van Veldhoven, Bart De Geest
Studies evaluating the effects of high-saturated fat diets on cardiac function are most often confounded by diet-induced obesity and by systemic insulin resistance. We evaluated whether coconut oil, containing C12:0 and C14:0 as main fatty acids, aggravates pressure overload-induced cardiomyopathy induced by transverse aortic constriction (TAC) in C57BL/6 mice. Mortality rate after TAC was higher (p < 0.05) in 0.2% cholesterol 10% coconut oil diet-fed mice than in standard chow-fed mice (hazard ratio 2.32, 95% confidence interval 1...
July 18, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28713936/epigallocatechin-gallate-attenuates-overload%C3%A2-induced-cardiac-ecm-remodeling-via-restoring-t-cell-homeostasis
#17
Yongsheng Han, Qingtong Wang, Xizhen Fan, Jun Chu, Junfu Peng, Yousheng Zhu, Yan Li, Xiaojing Li, Lei Shen, James Asenso, Shanfeng Li
It has previously been demonstrated that Epigallocatechin gallate (EGCG) has regulatory effects on cellular immunity. The present study explored whether EGCG inhibits the overload‑induced cardiac extracellular matrix (ECM) remodeling through targeting the balance of T cell subpopulations. Sprague‑Dawley rats were subjected to either transverse aortic constriction (TAC) or sham operation. TAC rats were treated with EGCG or valsartan (Val) for 6 weeks. The administration of EGCG or Val ameliorated the overproduction of cardiac collagen, inhibited matrix metalloproteinase (MMP) activity, decreased the expression of tissue inhibitor of MMP‑2, atrial natriuretic peptide and brain natriuretic peptide...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28708271/melatonin-protects-against-the-pathological-cardiac-hypertrophy-induced-by-transverse-aortic-constriction-through-activating-pgc-1%C3%AE-in-vivo-and-in-vitro-studies
#18
Mengen Zhai, Zhenhua Liu, Bin Zhang, Lin Jing, Buying Li, Kaifeng Li, Xiuju Chen, Meng Zhang, Bo Yu, Kai Ren, Yang Yang, Wei Yi, Jian Yang, Jincheng Liu, Dinghua Yi, Hongliang Liang, Zhenxiao Jin, Russel J Reiter, Weixun Duan, Shiqiang Yu
Melatonin, a circadian molecule secreted by the pineal gland, confers a protective role against cardiac hypertrophy induced by hyperthyroidism, chronic hypoxia, and isoproterenol. However, its role against pressure overload-induced cardiac hypertrophy and the underlying mechanisms remains elusive. In this study, we investigated the pharmacological effects of melatonin on pathological cardiac hypertrophy induced by transverse aortic constriction (TAC). Male C57BL/6 mice underwent TAC or sham surgery at day 0 and were then treated with melatonin (20 mg/kg/day, via drinking water) for 4 or 8 weeks...
July 14, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28667250/heart-failure-and-mef2-transcriptome-dynamics-in-response-to-%C3%AE-blockers
#19
S W Tobin, S Hashemi, K Dadson, S Turdi, K Ebrahimian, J Zhao, G Sweeney, J Grigull, J C McDermott
Myocyte Enhancer Factor 2 (MEF2) mediates cardiac remodelling in heart failure (HF) and is also a target of β-adrenergic signalling, a front-line treatment for HF. We identified global gene transcription networks involved in HF with and without β-blocker treatment. Experimental HF by transverse aortic constriction (TAC) in a MEF2 "sensor" mouse model (6 weeks) was followed by four weeks of β-blockade with Atenolol (AT) or Solvent (Sol) treatment. Transcriptome analysis (RNA-seq) from left ventricular RNA samples and MEF2A depleted cardiomyocytes was performed...
June 30, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28667100/interleukin-10-inhibits-bone-marrow-fibroblast-progenitor-cell-mediated-cardiac-fibrosis-in-pressure-overloaded-myocardium
#20
Suresh K Verma, Venkata N S Garikipati, Prasanna Krishnamurthy, Sarah M Schumacher, Laurel A Grisanti, Maria Cimini, Zhongjian Cheng, Mohsin Khan, Yujia Yue, Cindy Benedict, May M Truongcao, Joseph E Rabinowitz, David A Goukassian, Douglas Tilley, Walter J Koch, Raj Kishore
BACKGROUND: Activated fibroblasts (myofibroblasts) play a critical role in cardiac fibrosis; however, their origin in the diseased heart remains unclear, warranting further investigation. Recent studies suggest the contribution of bone marrow fibroblast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis. We have previously shown that interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the role of IL10 in inhibition of BM-FPC-mediated cardiac fibrosis is not known...
September 5, 2017: Circulation
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