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Transverse aortic constriction

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https://www.readbyqxmd.com/read/29792884/pharmacological-inhibition-of-dna-methylation-attenuates-pressure-overload-induced-cardiac-hypertrophy-in-rats
#1
Justus Stenzig, Yvonne Schneeberger, Alexandra Löser, Barbara S Peters, Andreas Schaefer, Rong-Rong Zhao, Shi Ling Ng, Grit Höppner, Birgit Geertz, Marc N Hirt, Wilson Tan, Eleanor Wong, Hermann Reichenspurner, Roger S-Y Foo, Thomas Eschenhagen
BACKGROUND: Heart failure is associated with altered gene expression and DNA methylation. De novo DNA methylation is associated with gene silencing, but its role in cardiac pathology remains incompletely understood. We hypothesized that inhibition of DNA methyltransferases (DNMT) might prevent the deregulation of gene expression and the deterioration of cardiac function under pressure overload (PO). To test this hypothesis, we evaluated a DNMT inhibitor in PO in rats and analysed DNA methylation in cardiomyocytes...
May 21, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29790114/ivabradine-improved-left-ventricular-function-and-pressure-overload-induced-cardiomyocyte-apoptosis-in-a-transverse-aortic-constriction-mouse-model
#2
Yihui Yu, Zuoying Hu, Bing Li, Zhimei Wang, Shaoliang Chen
This study aimed to investigate the effects and molecular mechanisms of ivabradine in preventing cardiac hypertrophy in an established transverse aortic constriction (TAC) mouse model. A total of 56 male C57BL/6 mice were randomly assigned into the following seven groups (8 mice per group): sham, TAC model, Iva-10 (10 mg/kg/day ivabradine), Iva-20 (20 mg/kg/day ivabradine), Iva-40 (40 mg/kg/day ivabradine), Iva-80 (80 mg/kg/day ivabradine), and Rap (rapamycin, a positive control). Echocardiography and left ventricular hemodynamics were performed...
May 22, 2018: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/29786048/cardiac-hypertrophy-is-positively-regulated-by-microrna%C3%A2-24-in-rats
#3
Juan Gao, Min Zhu, Rui-Feng Liu, Jian-Shu Zhang, Ming Xu
Background: MicroRNA-24 (miR-24) plays an important role in heart failure by reducing the efficiency of myocardial excitation-contraction coupling. Prolonged cardiac hypertrophy may lead to heart failure, but little is known about the role of miR-24 in cardiac hypertrophy. This study aimed to preliminarily investigate the function of miR-24 and its mechanisms in cardiac hypertrophy. Methods: Twelve Sprague-Dawley rats with a body weight of 50 ± 5 g were recruited and randomly divided into two groups: a transverse aortic constriction (TAC) group and a sham surgery group...
June 5, 2018: Chinese Medical Journal
https://www.readbyqxmd.com/read/29772440/inhibition-of-nogo-b-promotes-cardiac-hypertrophy-via-endoplasmic-reticulum-stress
#4
Junli Li, Wenchao Wu, Yanguo Xin, Mingyue Zhao, Xiaojing Liu
AIMS: Nogo-B is a key endoplasmic reticulum (ER) protein that regulates ER stress signaling. However, its role in cardiac hypertrophy remains poorly understood. ER stress is interrelated with autophagy in the process of cardiac hypertrophy. Therefore, we aimed to test the hypothesis that both ER stress and autophagy signaling mediate the function of Nogo-B in cardiac hypertrophy. MAIN METHODS: Rat models of transverse aortic constriction (TAC), neonatal rat cardiomyocytes (NRCMs) stimulated with norepinephrine (Ne) and primary cardiac fibroblasts treated with transforming growth factor β1 (TGF-β1) were used in this study...
May 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29771428/ampk-regulates-energy-metabolism-through-the-sirt1-signaling-pathway-to-improve-myocardial-hypertrophy
#5
H-W Dong, L-F Zhang, S-L Bao
OBJECTIVE: We investigated the correlations of adenosine monophosphate-activated protein kinase (AMPK), Silence information regulator 1 (SIRT1) and energy metabolism with myocardial hypertrophy. MATERIALS AND METHODS: Myocardial hypertrophy experimental model was established via transverse aortic constriction (TAC)-induced myocardial hypertrophy and phenylephrine (PE)-induced hypertrophic myocardial cell culture. After activation of AMPK, the messenger ribonucleic acid (mRNA) expressions in myocardial tissue- and myocardial cell hypertrophy-related genes, atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MHC), were detected...
May 2018: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/29751971/cardiac-hypertrophy-elevates-serum-levels-of-fibroblast-growth-factor-23
#6
Isao Matsui, Tatsufumi Oka, Yasuo Kusunoki, Daisuke Mori, Nobuhiro Hashimoto, Ayumi Matsumoto, Karin Shimada, Satoshi Yamaguchi, Keiichi Kubota, Sayoko Yonemoto, Tomoaki Higo, Yusuke Sakaguchi, Yoshitsugu Takabatake, Takayuki Hamano, Yoshitaka Isaka
Several experimental studies have shown that fibroblast growth factor 23 (FGF23) induces left ventricular hypertrophy (LVH). However, the opposite directional relationship, namely a potential effect of LVH on FGF23, remains uncertain. Here we evaluated the effects of LVH on FGF23 using cardiomyocyte-specific calcineurin A transgenic mice. At six weeks, these mice showed severe LVH, with elevated levels of serum intact FGF23. FGF23 levels were elevated in cardiomyocytes, but not osteocytes, of the transgenic animals...
May 8, 2018: Kidney International
https://www.readbyqxmd.com/read/29744294/synergistic-effects-of-hmg-coa-reductase-inhibitor-and-angiotensin-ii-receptor-blocker-on-load-induced-heart-failure
#7
Yusuke Ito, Yasuhiro Maejima, Natsuko Tamura, Yuka Shiheido-Watanabe, Masanori Konishi, Takashi Ashikaga, Kenzo Hirao, Mitsuaki Isobe
5-Hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) have beneficial effects in patients with heart failure (HF), regardless of serum cholesterol levels. However, their synergic effects with angiotensin II receptor blocker (ARB) remain to be established. We assessed the existence and potential underlying mechanisms of the effects of combined ARB [losartan (LOS)] and statin [simvastatin (SIM)] on cardiac function in rats and mice with load-induced HF. Salt-loaded Dahl salt-sensitive (DS) rats were treated with vehicle, LOS, SIM, or LOS + SIM for 8 weeks...
May 2018: FEBS Open Bio
https://www.readbyqxmd.com/read/29729330/paraoxonase-2-prevents-the-development-of-heart-failure
#8
Wei Li, David Kennedy, Zhili Shao, Xi Wang, Andre Klaassen Kamdar, Malory Weber, Kayla Mislick, Kathryn Kiefer, Rommel Morales, Brendan Agatisa-Boyle, Diana M Shih, Srinivasa T Reddy, Christine S Moravec, W H Wilson Tang
BACKGROUND: Mitochondrial oxidation is a major source of reactive oxygen species (ROS) and mitochondrial dysfunction plays a central role in development of heart failure (HF). Paraoxonase 2 deficient (PON2-def) mitochondria are impaired in function. In this study, we tested whether PON2-def aggravates HF progression. METHODS AND RESULTS: Using qPCR, immunoblotting and lactonase activity assay, we demonstrate that PON2 activity was significantly decreased in failing hearts despite increased PON2 expression...
May 2, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29721099/microrna-378-suppresses-myocardial-fibrosis-through-a-paracrine-mechanism-at-the-early-stage-of-cardiac-hypertrophy-following-mechanical-stress
#9
Jie Yuan, Haibo Liu, Wei Gao, Li Zhang, Yong Ye, Lingyan Yuan, Zhiwen Ding, Jian Wu, Le Kang, Xiaoyi Zhang, Xiaoyan Wang, Guoping Zhang, Hui Gong, Aijun Sun, Xiangdong Yang, Ruizhen Chen, Zhaoqiang Cui, Junbo Ge, Yunzeng Zou
Rationale : Excessive myocardial fibrosis is the main pathological process in the development of cardiac remodeling and heart failure; therefore, it is important to prevent excessive myocardial fibrosis. We determined that microRNA-378 (miR-378) is cardiac-enriched and highly repressed during cardiac remodeling. We therefore proposed that miR-378 has a critical role in regulation of cardiac fibrosis, and examined the effects of miR-378 on cardiac fibrosis after mechanical stress. Methods: Mechanical stress was respectively imposed on mice through a transverse aortic constriction (TAC) procedure and on cardiac fibroblasts by stretching silicon dishes...
2018: Theranostics
https://www.readbyqxmd.com/read/29716898/load-dependent-changes-in-left-ventricular-structure-and-function-in-a-pathophysiologically-relevant-murine-model-of-reversible-heart-failure
#10
Carla J Weinheimer, Attila Kovacs, Sarah Evans, Scot J Matkovich, Philip M Barger, Douglas L Mann
BACKGROUND: To better understand reverse left ventricular (LV) remodeling, we developed a murine model wherein mice develop LV remodeling after transverse aortic constriction (TAC) and a small apical myocardial infarct (MI) and undergo reverse LV remodeling after removal of the aortic band. METHODS AND RESULTS: Mice studied were subjected to sham (n=6) surgery or TAC+MI (n=12). Two weeks post-TAC+MI, 1 group underwent debanding (referred to as heart failure debanding [HF-DB] mice; n=6), whereas the aortic band remained in a second group (heart failure [HF] group; n=6)...
May 2018: Circulation. Heart Failure
https://www.readbyqxmd.com/read/29688911/tranilast-blunts-the-hypertrophic-and-fibrotic-response-to-increased-afterload-independent-of-cardiomyocyte-transient-receptor-potential-vanilloid-2-channels
#11
Sheryl E Koch, Michelle L Nieman, Nathan Robbins, Samuel Slone, Mariah Worley, Lisa C Green, Yamei Chen, Alexandria Barlow, Michael Tranter, HongSheng Wang, John N Lorenz, Jack Rubinstein
Tranilast is clinically indicated for the treatment of allergic disorders and is also a non-selective blocker of the Transient Receptor Potential Vanilloid 2 (TRPV2) channel. Prior studies have found that it has protective effects in various animal models of cardiac disease. Our laboratory has found that genetic deletion of TRPV2 results in a blunted hypertrophic response to increased afterload, thus this study tested the hypothesis that tranilast through cardiomyocyte TRPV2 blockade can inhibit the hypertrophic response to pressure overload in-vivo via transverse aortic constriction and ex vivo via isolated myocyte studies...
April 20, 2018: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/29683463/a-closed-chest-model-to-induce-transverse-aortic-constriction-in-mice
#12
Lars Eichhorn, Christina Katharina Weisheit, Christopher Gestrich, Konrad Peukert, Georg Daniel Duerr, Muhammad Ajmal Ayub, Felix Erdfelder, Florian Stöckigt
Research on cardiac hypertrophy and heart failure is frequently based on pressure overload mouse models induced by TAC. The standard procedure is to perform a partial thoracotomy to visualize the transverse aortic arch. However, the surgical trauma caused by the thoracotomy in open-chest models changes the respiratory physiology as the ribs are dissected and left unattached after chest closure. To prevent this, we established a minimally invasive, closed chest approach via lateral thoracotomy. Herein we approach the aortic arch via the 2nd intercostal space without entering the chest cavities, leaving the mouse with a less traumatic injury to recover from...
April 5, 2018: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/29678661/role-of-heat-shock-transcription-factor-1-hsf1-upregulated-macrophage-in-ameliorating-pressure-overload-induced-heart-failure-in-mice
#13
Peizhao Du, Yaowei Chang, Fangjie Dai, Chunyan Wei, Qi Zhang, Jiming Li
In order to explore the role of macrophages in HSF1-mediated alleviation of heart failure, mice model of pressure overload-induced heart failure was established using transverse aortic constriction (TAC). Changes in cardiac function and morphology were studied in TAC and SHAM groups using ultrasonic device, tissue staining, electron microscopy, real-time quantitative polymerase chain reaction (RT-QPCR), and Western blotting. We found that mice in the TAC group showed evidence of impaired cardiac function and aggravation of fibrosis on ultrasonic and histopathological examination when compared to those in the SHAM group...
April 17, 2018: Gene
https://www.readbyqxmd.com/read/29669786/rearrangement-of-the-protein-phosphatase-1-interactome-during-heart-failure-progression
#14
David Y Chiang, Katherina M Alsina, Eleonora Corradini, Martin Fitzpatrick, Li Ni, Satadru K Lahiri, Julia Reynolds, Xiaolu Pan, Larry Scott, Albert J R Heck, Xander H Wehrens
Background -Heart failure (HF) is a complex disease with a rising prevalence despite advances in treatment. Protein phosphatase 1 (PP1) has long been implicated in HF pathogenesis but its exact role is both unclear and controversial. Most previous studies measured only the PP1 catalytic subunit (PP1c) without investigating its diverse set of interactors, which confer localization and substrate specificity to the holoenzyme. In this study we define the PP1 interactome in cardiac tissue and test the hypothesis that this interactome becomes rearranged during HF progression at the level of specific PP1c interactors...
April 18, 2018: Circulation
https://www.readbyqxmd.com/read/29666587/cardioprotective-effects-of-qishenyiqi-dripping-pills-on-transverse-aortic-constriction-induced-heart-failure-in-mice
#15
Guoran Ruan, Haojin Ren, Chi Zhang, Xiaogang Zhu, Chao Xu, Liyue Wang
QiShenYiQi dripping pills (QSYQ), a traditional Chinese medicine, are commonly used to treat coronary heart disease, and QSYQ was recently approved as a complementary treatment for ischemic heart failure in China. However, only few studies reported on whether QSYQ exerts a protective effect on heart failure induced by pressure overload. In this study, we explored the role of QSYQ in a mouse model of heart failure induced by transverse aortic constriction (TAC). Twenty-eight C57BL/6J mice were divided into four groups: Sham + NS group, Sham + QSYQ group, TAC + NS group, and TAC + QSYQ group...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29627295/deficiency-of-aldose-reductase-exacerbates-early-pressure-overload-induced-cardiac-dysfunction-and-autophagy-in-mice
#16
Shahid P Baba, Deqing Zhang, Mahavir Singh, Sujith Dassanayaka, Zhengzhi Xie, Ganapathy Jagatheesan, Jingjing Zhao, Virginia K Schmidtke, Kenneth R Brittian, Michael L Merchant, Daniel J Conklin, Steven P Jones, Aruni Bhatnagar
Pathological cardiac hypertrophy is associated with the accumulation of lipid peroxidation-derived aldehydes such as 4-hydroxy-trans-2-nonenal (HNE) and acrolein in the heart. These aldehydes are metabolized via several pathways, of which aldose reductase (AR) represents a broad-specificity route for their elimination. We tested the hypothesis that by preventing aldehyde removal, AR deficiency accentuates the pathological effects of transverse aortic constriction (TAC). We found that the levels of AR in the heart were increased in mice subjected to TAC for 2 weeks...
April 5, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29626503/hsf1-deficiency-accelerates-the-transition-from-pressure-overload-induced-cardiac-hypertrophy-to-heart-failure-through-endothelial-mir-195a-3p-mediated-impairment-of-cardiac-angiogenesis
#17
Shijun Wang, Jian Wu, Jieyun You, Hongyu Shi, Xiaoyu Xue, Jiayuan Huang, Lei Xu, Guoliang Jiang, Lingyan Yuan, Xue Gong, Haiyan Luo, Junbo Ge, Zhaoqiang Cui, Yunzeng Zou
Heat shock transcription factor 1 (HSF1) deficiency aggravates cardiac remodeling under pressure overload. However, the mechanism is still unknown. Here we employed microRNA array analysis of the heart tissue of HSF1-knockout (KO) mice to investigate the potential roles of microRNAs in pressure overload-induced cardiac remodeling under HSF-1 deficiency, and the profiles of 478 microRNAs expressed in the heart tissues of adult HSF1-KO mice were determined. We found that the expression of 5 microRNAs was over 2-fold higher expressed in heart tissues of HSF1-KO mice than in those of wild-type (WT) control mice...
April 4, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29621314/sildenafil-ameliorates-right-ventricular-early-molecular-derangement-during-left-ventricular-pressure-overload
#18
Yousuke Imai, Taro Kariya, Masaki Iwakiri, Yoshitsugu Yamada, Eiki Takimoto
Right ventricular (RV) dysfunction following left ventricular (LV) failure is associated with poor prognosis. RV remodeling is thought initiated by the increase in the afterload of RV due to secondary pulmonary hypertension (PH) to impaired LV function; however, RV molecular changes might occur in earlier stages of the disease. cGMP (cyclic guanosine monophosphate)-phosphodiesterase 5 (PDE5) inhibitors, widely used to treat PH through their pulmonary vasorelaxation properties, have shown direct cardiac benefits, but their impacts on the RV in LV diseases are not fully determined...
2018: PloS One
https://www.readbyqxmd.com/read/29616999/lncrna-uca1-is-a-novel-regulator-in-cardiomyocyte-hypertrophy-through-targeting-the-mir-184-hoxa9-axis
#19
Gaoliang Zhou, Chao Li, Jun Feng, Jing Zhang, Yanyan Fang
Cardiac hypertrophy is closely associated with a series of cardiovascular diseases, including heart failure and sudden death in particular. An in-depth comprehension of the pathogenesis of cardiac hypertrophy will improve the diagnosis and therapy of cardiac hypertrophy. It has been acknowledged that long noncoding RNAs/microRNAs (lncRNAs/miRNAs) are crucial regulators in diverse biological processes, including various cardiovascular diseases, in multiple manners. Nevertheless, the biological roles of lncRNA UCA1 and miR-184 in cardiac hypertrophy are scarcely reported...
2018: Cardiorenal Medicine
https://www.readbyqxmd.com/read/29555642/protective-roles-of-interferon-%C3%AE-in-cardiac-hypertrophy-induced-by-sustained-pressure-overload
#20
Akihiko Kimura, Yuko Ishida, Machi Furuta, Mizuho Nosaka, Yumi Kuninaka, Akira Taruya, Naofumi Mukaida, Toshikazu Kondo
BACKGROUND: A clear understanding of the molecular mechanisms underlying hemodynamic stress-initiated cardiac hypertrophy is important for preventing heart failure. Interferon-γ (IFN-γ) has been suggested to play crucial roles in various diseases other than immunological disorders by modulating the expression of myriad genes. However, the involvement of IFN-γ in the pathogenesis of cardiac hypertrophy still remains unclear. METHODS AND RESULTS: In order to elucidate the roles of IFN-γ in pressure overload-induced cardiac pathology, we subjected Balb/c wild-type (WT) or IFN-γ-deficient ( Ifng -/- ) mice to transverse aortic constriction (TAC)...
March 19, 2018: Journal of the American Heart Association
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