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https://www.readbyqxmd.com/read/27915452/chronic-enalapril-treatment-increases-transient-outward-potassium-current-in-cardiomyocytes-isolated-from-right-ventricle-of-spontaneously-hypertensive-rats
#1
Luiz Fernando Rodrigues Junior, Ana Carolina de Azevedo Carvalho, Enildo Broetto Pimentel, José Geraldo Mill, José Hamilton Matheus Nascimento
It has been well established that chronic pressure overload resulting from hypertension leads to ventricular hypertrophy and electrophysiological remodeling. The transient outward potassium current (I to) reduction described in hypertensive animals delays ventricular repolarization, leading to complex ventricular arrhythmias and sudden death. Antihypertensive drugs, as angiotensin-converting enzyme inhibitors (ACEi), can restore I to and reduce the incidence of arrhythmic events. The purpose of this study was to evaluate the differential effects of long-term treatment with ACEi or direct-acting smooth muscle relaxant on the I to of left and right ventricle myocytes of spontaneously hypertensive rats (SHR)...
December 3, 2016: Naunyn-Schmiedeberg's Archives of Pharmacology
https://www.readbyqxmd.com/read/27915400/the-pathophysiological-role-of-nox2-in-hypertension-and-organ-damage
#2
REVIEW
Maurizio Forte, Cristina Nocella, Elena De Falco, Silvia Palmerio, Leonardo Schirone, Valentina Valenti, Giacomo Frati, Roberto Carnevale, Sebastiano Sciarretta
NADPH oxidases (NOXs) represent one of the major sources of reactive oxygen species in the vascular district. Reactive oxygen species are responsible for vascular damage that leads to several cardiovascular pathological conditions. Among NOX isoforms, NOX2 is widely expressed in many cells types, such as cardiomyocytes, endothelial cells, and vascular smooth muscle cells, confirming its pivotal role in vascular pathophysiology. Studies in mice models with systemic deletion of NOX2, as well as in transgenic mice overexpressing NOX2, have demonstrated the undeniable involvement of NOX2 in the development of hypertension, atherosclerosis, diabetes mellitus, cardiac hypertrophy, platelet aggregation, and aging...
December 3, 2016: High Blood Pressure & Cardiovascular Prevention: the Official Journal of the Italian Society of Hypertension
https://www.readbyqxmd.com/read/27914791/aberrant-developmental-titin-splicing-and-dysregulated-sarcomere-length-in-thymosin-%C3%AE-4-knockout-mice
#3
Nicola Smart, Johannes Riegler, Cameron W Turtle, Craig A Lygate, Debra J McAndrew, Katja Gehmlich, Karina N Dubé, Anthony N Price, Vivek Muthurangu, Andrew M Taylor, Mark F Lythgoe, Charles Redwood, Paul R Riley
Sarcomere assembly is a highly orchestrated and dynamic process which adapts, during perinatal development, to accommodate growth of the heart. Sarcomeric components, including titin, undergo an isoform transition to adjust ventricular filling. Many sarcomeric genes have been implicated in congenital cardiomyopathies, such that understanding developmental sarcomere transitions will inform the aetiology and treatment. We sought to determine whether Thymosin β4 (Tβ4), a peptide that regulates the availability of actin monomers for polymerization in non-muscle cells, plays a role in sarcomere assembly during cardiac morphogenesis and influences adult cardiac function...
November 30, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27913938/cardiotoxic-and-dyslipidemic-effects-of-doxorubicin-and-betulinic-acid-amide
#4
M G Klinnikova, E L Lushnikova, E V Koldysheva, T G Tolstikova, I V Sorokina, E I Yuzhik, M M Mzhelskaya
Changes in the blood lipid spectrum and structural reorganization of the rat myocardium in response to injection of a single sublethal dose of doxorubicin (7 mg/kg) alone and in combination with course administration of betulonic acid amide (100 mg/kg/day for 14 days) were studied. Betulinic acid amide in the specified dose exhibited less pronounced cardiotoxic (necrobiotic impairment of cardiomyocytes) and dyslipidemic (increase of cholesterol and triglyceride levels) effects in comparison with doxorubicin...
December 3, 2016: Bulletin of Experimental Biology and Medicine
https://www.readbyqxmd.com/read/27913823/mathematical-models-suggest-facilitated-fatty-acids-crossing-of-the-luminal-membrane-in-the-cardiac-muscle
#5
Efrath Barta
Long-chain fatty acids cross a few membranes on their way from the capillary blood to the cardiomyocyte cytosol, where they are utilized as an essential source of energy. Details of the transport mechanism across those membranes remained elusive despite decades of laboratory and theoretical work. Here we inspect several optional scenarios for the crossing of the luminal membrane of the endothelial cell, the first barrier that should be crossed: a passive diffusion, facilitation by receptors for albumin and facilitation by fatty acids transporters...
December 3, 2016: Journal of Membrane Biology
https://www.readbyqxmd.com/read/27913284/cardiac-proteasome-functional-insufficiency-plays-a-pathogenic-role-in-diabetic-cardiomyopathy
#6
Jie Li, Wenxia Ma, Guihua Yue, Yaoliang Tang, Il-Man Kim, Neal L Weintraub, Xuejun Wang, Huabo Su
BACKGROUND: Diabetic cardiomyopathy is a major risk factor in diabetic patients but its pathogenesis remains poorly understood. The ubiquitin-proteasome system (UPS) facilitates protein quality control by degrading unnecessary and damaged proteins in eukaryotic cells, and dysfunction of UPS is implicated in various cardiac diseases. However, the overall functional status of the UPS and its pathophysiological role in diabetic cardiomyopathy have not been determined. METHODS AND RESULTS: Type I diabetes was induced in wild-type and transgenic mice expressing a UPS functional reporter (GFPdgn) by injections of streptozotocin (STZ)...
November 29, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27912208/smad-nuclear-interacting-protein-1-acts-as-a-protective-regulator-of-pressure-overload-induced-pathological-cardiac-hypertrophy
#7
Yu-Yan Lu, Da-Chun Xu, Yi-Fan Zhao, Guo-Fu Zhu, Meng-Yun Zhu, Wei-Jing Liu, Xue-Jing Yu, Wei Chen, Zheng Liu, Ya-Wei Xu
BACKGROUND: Smad nuclear interacting protein 1 (SNIP1) plays a critical role in cell proliferation, transformation of embryonic fibroblasts, and immune regulation. However, the role of SNIP1 in cardiac hypertrophy remains unclear. METHODS AND RESULTS: Here we examined the role of SNIP1 in pressure overload-induced cardiac hypertrophy and its mechanisms. Our results demonstrated that SNIP1 expression was downregulated in human dilated cardiomyopathic hearts, aortic banding-induced mice hearts, and angiotensin II-treated cardiomyocytes...
October 26, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27911738/can-the-drosophila-model-help-in-paving-the-way-for-translational-medicine-in-heart-failure
#8
REVIEW
Lisha Ma
Chronic heart failure is a common consequence of various heart diseases. Mechanical force is known to play a key role in heart failure development through regulating cardiomyocyte hypertrophy. In order to understand the complex disease mechanism, this article discussed a multi-disciplinary approach that may aid the illustration of heart failure molecular process.
October 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27911441/sirt1-protects-the-heart-from-er-stress-induced-cell-death-through-eif2%C3%AE-deacetylation
#9
Alexandre Prola, Julie Pires Da Silva, Arnaud Guilbert, Lola Lecru, Jérôme Piquereau, Maxance Ribeiro, Philippe Mateo, Mélanie Gressette, Dominique Fortin, Céline Boursier, Cindy Gallerne, Anaïs Caillard, Jane-Lise Samuel, Hélène François, David A Sinclair, Pierre Eid, Renée Ventura-Clapier, Anne Garnier, Christophe Lemaire
Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective...
December 2, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27911047/modified-mrna-as-a-therapeutic-tool-to-induce-cardiac-regeneration-in-ischemic-heart-disease
#10
REVIEW
Yoav Hadas, Michael G Katz, Charles R Bridges, Lior Zangi
Ischemic heart disease (IHD) is a leading cause of morbidity and mortality in developed countries. Current pharmacological and interventional therapies provide significant improvement in the life quality of patient; however, they are mostly symptom-oriented and not curative. A high disease and economic burden of IHD requires the search for new therapeutic strategies to significantly improve patients' prognosis and quality of life. One of the main challenges during IHD is the massive loss of cardiomyocytes that possess minimal regenerative capacity...
December 2, 2016: Wiley Interdisciplinary Reviews. Systems Biology and Medicine
https://www.readbyqxmd.com/read/27911036/properties-of-embryoid-bodies
#11
REVIEW
Joshua M Brickman, Palle Serup
Embryoid bodies (EBs) have been popular in vitro differentiation models for pluripotent stem cells for more than five decades. Initially, defined as aggregates formed by embryonal carcinoma cells, EBs gained more prominence after the derivation of karyotypically normal embryonic stem cells from early mouse blastocysts. In many cases, formation of EBs constitutes an important initial step in directed differentiation protocols aimed at generated specific cell types from undifferentiated stem cells. Indeed state-of-the-art protocols for directed differentiation of cardiomyocytes still rely on this initial EB step...
December 2, 2016: Wiley Interdisciplinary Reviews. Developmental Biology
https://www.readbyqxmd.com/read/27910058/gene-delivery-for-the-generation-of-bioartificial-pacemaker
#12
Patrick K W Chan, Ronald A Li
Electronic pacemakers have been used in patients with heart rhythm disorders for device-supported pacing. While effective, there are such shortcomings as limited battery life, permanent implantation of catheters, the lack of autonomic neurohumoral responses, and risks of lead dislodging. Here we describe protocols for establishing porcine models of sick sinus syndrome and complete heart block, and the generation of bioartificial pacemaker by delivering a strategically engineered form of hyperpolarization-activated cyclic nucleotide-gated pacemaker channel protein via somatic gene transfer to convert atrial or ventricular muscle cardiomyocytes into nodal-like cells that rhythmically fire action potentials...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27910055/selective-pressure-regulated-retroinfusion-for-gene-therapy-application-in-ischemic-heart-disease
#13
Rabea Hinkel, Christian Kupatt
Coronary heart disease is still the leading cause of death in industrialized nations. Even though revascularization strategies such as coronary artery bypass graft surgery, percutaneous coronary intervention and enhanced drug therapy significantly improved the outcome, about 30 % of patients develop chronic heart failure. Ischemic heart disease and heart failure are characterized by an adverse remodeling of the heart, featuring cardiomyocyte hypertrophy, increased fibrosis and capillary rarefaction. Therefore, gene therapeutic approaches for the treatment of heart failure, such as the modulating contractile function or therapeutic neovascularization, seem to be promising...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27910049/gene-transfer-in-cardiomyocytes-derived-from-es-and-ips-cells
#14
Francesca Stillitano, Ioannis Karakikes, Roger J Hajjar
The advent of human induced pluripotent stem cell (hiPSC) technology has produced patient-specific hiPSC derived cardiomyocytes (hiPSC-CMs) that can be used as a platform to study cardiac diseases and to explore new therapies.The ability to genetically manipulate hiPSC-CMs not only is essential for identifying the structural and/or functional role of a protein but can also provide valuable information regarding therapeutic applications. In this chapter, we describe protocols for culture, maintenance, and cardiac differentiation of hiPSCs...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27910048/gene-transfer-in-isolated-adult-cardiomyocytes
#15
Kjetil Hodne, David B Lipsett, William E Louch
During the past few decades, gene delivery using recombinant virus has made tremendous progress. With a higher than 80 % transduction efficiency, even in non-dividing cells, viral transduction has become the method of choice for efficient gene transfer into cardiomyocytes. However, in vitro gene delivery is dependent on a robust cell isolation protocol, as prolonged cultivation is needed to initiate gene expression and target specific cellular processes. This chapter describes some of the important steps that need to be considered for successful in vitro gene transfer into adult cardiomyocytes...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27910043/production-and-characterization-of-vectors-based-on-the-cardiotropic-aav-serotype-9
#16
Erik Kohlbrenner, Thomas Weber
Vectors based on adeno-associated virus serotype 9 (AAV9) efficiently transduce cardiomyocytes in both rodents and large animal models upon either systemic or regional vector delivery. In this chapter, we describe the most widely used production and purification method of AAV9. This production approach does not depend on the use of a helpervirus but instead on transient transfection of HEK293T cells with a plasmid containing the recombinant AAV genome and a second plasmid encoding the AAV9 capsid proteins, the AAV Rep proteins and the adenoviral helper functions...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27910042/direct-cardiac-reprogramming-as-a-novel-therapeutic-strategy-for-treatment-of-myocardial-infarction
#17
Hong Ma, Li Wang, Jiandong Liu, Li Qian
Direct reprogramming of fibroblasts into induced cardiomyocytes (iCMs) holds great promise as a novel therapy for the treatment of heart failure, a common and morbid disease that is usually caused by irreversible loss of functional cardiomyocytes (CMs). Recently, we and others showed that in a murine model of acute myocardial infarction, delivery of three transcription factors, Gata4, Mef2c, and Tbx5 converted endogenous cardiac fibroblasts into functional iCMs. These iCMs integrated electrically and mechanically with surrounding myocardium, resulting in a reduction in scar size and an improvement in heart function...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27910039/silencing-genes-in-the-heart
#18
Henry Fechner, Roland Vetter, Jens Kurreck, Wolfgang Poller
Silencing of cardiac genes by RNA interference (RNAi) has developed into a powerful new method to treat cardiac diseases. Small interfering (si)RNAs are the inducers of RNAi, but cultured primary cardiomyocytes and heart are highly resistant to siRNA transfection. This can be overcome by delivery of small hairpin (sh)RNAs or artificial microRNA (amiRNAs) by cardiotropic adeno-associated virus (AAV) vectors. Here we describe as example of the silencing of a cardiac gene, the generation and cloning of shRNA, and amiRNAs directed against the cardiac protein phospholamban...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27909533/patient-specific-induced-pluripotent-stem-cell-derived-cardiomyocytes-for-drug-development-and-screening-in-catecholaminergic-polymorphic-ventricular-tachycardia
#19
REVIEW
Ben Jehuda Ronen, Barad Lili
Catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited arrhythmia often leading to sudden cardiac death in children and young adults, is characterized by polymorphic/bidirectional ventricular tachycardia induced by adrenergic stimulation associated with emotionally stress or physical exercise. There are two forms of CPVT: 1. CPVT1 is caused by mutations in the RYR2 gene, encoding for ryanodine receptor type 2. CPVT1 is the most common form of CPVT in the population, and is inherited by a dominant mechanism...
August 2016: Journal of Atrial Fibrillation
https://www.readbyqxmd.com/read/27908661/uniform-low-level-dystrophin-expression-in-the-heart-partially-preserved-cardiac-function-in-an-aged-mouse-model-of-duchenne-cardiomyopathy
#20
Nalinda B Wasala, Yongping Yue, Jenna Vance, Dongsheng Duan
Dystrophin deficiency results in Duchenne cardiomyopathy, a primary cause of death in Duchenne muscular dystrophy (DMD). Gene therapy has shown great promise in ameliorating the cardiac phenotype in mouse models of DMD. However, it is not completely clear how much dystrophin is required to treat dystrophic heart disease. We and others have shown that mosaic dystrophin expression at the wild-type level, depending on the percentage of dystrophin positive cardiomyocytes, can either delay the onset of or fully prevent cardiomyopathy in dystrophin-null mdx mice...
November 28, 2016: Journal of Molecular and Cellular Cardiology
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