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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/28089740/early-remodeling-of-repolarizing-k-currents-in-the-%C3%AE-mhc-403-mouse-model-of-familial-hypertrophic-cardiomyopathy
#1
Rocco Hueneke, Adam Adenwala, Rebecca L Mellor, Jonathan G Seidman, Christine E Seidman, Jeanne M Nerbonne
Familial hypertrophic cardiomyopathy (HCM), linked to mutations in myosin, myosin-binding proteins and other sarcolemmal proteins, is associated with increased risk of life threatening ventricular arrhythmias, and a number of animal models have been developed to facilitate analysis of disease progression and mechanisms. In the experiments here, we use the αMHC(403/+) mouse line in which one αMHC allele harbors a common HCM mutation (in βMHC, Arg403 Gln). Here, we demonstrate marked prolongation of QT intervals in young adult (10-12week) male αMHC(403/+) mice, well in advance of the onset of measurable left ventricular hypertrophy...
January 12, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28088561/mutant-dd-genotype-of-nfkb1-gene-is-associated-with-the-susceptibility-and-severity-of-coronary-artery-disease
#2
Jun-Yi Luo, Xiao-Mei Li, Yun Zhou, Qiang Zhao, Bang-Dang Chen, Fen Liu, Xiao-Cui Chen, Hong Zheng, Yi-Tong Ma, Xiao-Ming Gao, Yi-Ning Yang
Nuclear factor κappa B (NF-κB) is an important transcription factor in the development and progression of coronary artery disease (CAD). Recent evidence suggests that -94 ATTG ins/del mutant in the promoter of NFKB1 gene is an essential functional mutant. The present study demonstrated the frequencies of the del/del (DD) genotype and del (D) allele were significantly higher in CAD patients than in controls. CAD patients carrying mutant DD genotype had worse stenosis of diseased coronary arteries compared to those carrying ins/ins (II) or ins/del (ID) genotype...
January 11, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28087265/myocardial-relaxation-is-accelerated-by-fast-stretch-not-reduced-afterload
#3
Charles S Chung, Charles W Hoopes, Kenneth S Campbell
Fast relaxation of cross-bridge generated force in the myocardium facilitates efficient diastolic function. Recently published research studying mechanisms that modulate the relaxation rate has focused on molecular factors. Mechanical factors have received less attention since the 1980s when seminal work established the theory that reducing afterload accelerates the relaxation rate. Clinical trials using afterload reducing drugs, partially based on this theory, have thus far failed to improve outcomes for patients with diastolic dysfunction...
January 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28077294/into-the-golden-anniversary-of-the-yellow-journal
#4
EDITORIAL
R John Solaro
No abstract text is available yet for this article.
January 8, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28077321/camkii%C3%AE-subtypes-differentially-regulate-infarct-formation-following-ex-vivo-myocardial-ischemia-reperfusion-through-nf-%C3%AE%C2%BAb-and-tnf-%C3%AE
#5
Charles B B Gray, Takeshi Suetomi, Sunny Xiang, Erik A Blackwood, Christopher C Glembotski, Shigeki Miyamoto, B Daan Westenbrink, Joan Heller Brown
Deletion of Ca(2+)/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been shown to protect against in vivo ischemia/reperfusion (I/R) injury. It remains unclear which CaMKIIδ isoforms and downstream mechanisms are responsible for the salutary effects of CaMKIIδ gene deletion. In this study we sought to compare the roles of the CaMKIIδB and CaMKIIδC subtypes and the mechanisms by which they contribute to ex vivo I/R damage. WT, CaMKIIδKO, and mice expressing only CaMKIIδB or δC were subjected to ex vivo global ischemia for 25min followed by reperfusion...
January 7, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28077320/serine-threonine-phosphatases-in-atrial-fibrillation
#6
Jordi Heijman, Shokoufeh Ghezelbash, Xander H T Wehrens, Dobromir Dobrev
Serine/threonine protein phosphatases control dephosphorylation of numerous cardiac proteins, including a variety of ion channels and calcium-handling proteins, thereby providing precise post-translational regulation of cardiac electrophysiology and function. Accordingly, dysfunction of this regulation can contribute to the initiation, maintenance and progression of cardiac arrhythmias. Atrial fibrillation (AF) is the most common heart rhythm disorder and is characterized by electrical, autonomic, calcium-handling, contractile, and structural remodeling, which include, among other things, changes in the phosphorylation status of a wide range of proteins...
January 7, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28065668/ablation-of-the-cardiac-ryanodine-receptor-phospho-site-ser2808-does-not-alter-the-adrenergic-response-or-the-progression-to-heart-failure-in-mice-elimination-of-the-genetic-background-as-critical-variable
#7
Francisco J Alvarado, Xi Chen, Héctor H Valdivia
BACKGROUND: Phosphorylation of the cardiac ryanodine receptor (RyR2) phospho-site S2808 has been touted by the Marks group as a hallmark of heart failure (HF) and a critical mediator of the physiological fight-or-flight response of the heart. In support of this hypothesis, mice unable to undergo phosphorylation at RyR2-S2808 (S2808A) were significantly protected against HF and displayed a blunted response to adrenergic stimulation. However, the issue remains highly controversial because several groups have been unable to reproduce these findings...
January 6, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28041873/il-33-enhances-macrophage-m2-polarization-and-protects-mice-from-cvb3-induced-viral-myocarditis
#8
Chao Wang, Chunsheng Dong, Sidong Xiong
Viral myocarditis is the inflammation caused by myocardial virus infection, and the coxsackievirus group B3 virus (CVB3) is the most common pathogen. An efficient therapeutic agent against viral myocarditis is currently unavailable. IL-33, a new member of the IL-1 cytokine superfamily, exhibits potential immunotherapeutic effect against inflammatory and autoimmune diseases. However, the functional role of IL-33 in viral myocarditis has not been investigated. To examine the therapeutic role of IL-33 in viral myocarditis, an IL-33 overexpression plasmid (pDisplay-IL-33) and IL-33 knockdown plasmid (pLL3...
December 29, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28025046/camkii-is-a-nodal-signal-for-multiple-programmed-cell-death-pathways-in-heart
#9
Ning Feng, Mark E Anderson
Sustained Ca(2+)/calmodulin dependent kinase II (CaMKII) activation plays a central role in the pathogenesis of a variety of cardiac diseases. Emerging evidence suggests CaMKII evoked programmed cell death, including apoptosis and necroptosis, is one of the key underlying mechanisms for the detrimental effect of sustained CaMKII activation. CaMKII integrates β-adrenergic, Gq coupled receptor, reactive oxygen species (ROS), hyperglycemia, and pro-death cytokine signaling to elicit myocardial apoptosis by intrinsic and extrinsic pathways...
December 23, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28017639/selective-coupling-of-the-s1p3-receptor-subtype-to-s1p-mediated-rhoa-activation-and-cardioprotection
#10
Bryan S Yung, Cameron S Brand, Sunny Y Xiang, Charles B B Gray, Christopher K Means, Hugh Rosen, Jerold Chun, Nicole H Purcell, Joan Heller Brown, Shigeki Miyamoto
Sphingosine-1-phosphate (S1P), a bioactive lysophospholipid, is generated and released at sites of tissue injury in the heart and can act on S1P1, S1P2, and S1P3 receptor subtypes to affect cardiovascular responses. We established that S1P causes little phosphoinositide hydrolysis and does not induce hypertrophy indicating that it does not cause receptor coupling to Gq. We previously demonstrated that S1P confers cardioprotection against ischemia/reperfusion by activating RhoA and its downstream effector PKD...
December 23, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28007541/calcineurin-signaling-in-the-heart-the-importance-of-time-and-place
#11
Valentina Parra, Beverly A Rothermel
The calcium-activated protein phosphatase, calcineurin, lies at the intersection of protein phosphorylation and calcium signaling cascades, where it provides an essential nodal point for coordination between these two fundamental modes of intracellular communication. In excitatory cells, such as neurons and cardiomyocytes, that experience rapid and frequent changes in cytoplasmic calcium, calcineurin protein levels are exceptionally high, suggesting that these cells require high levels of calcineurin activity...
December 20, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27993561/loss-of-smooth-muscle-cell-disintegrin-and-metalloproteinase-17-transiently-suppresses-angiotensin-ii-induced-hypertension-and-end-organ-damage
#12
Mengcheng Shen, Jude Morton, Sandra T Davidge, Zamaneh Kassiri
Hypertension is associated with hypertrophy and hyperplasia of smooth muscle cells (SMCs). Disintegrin and metalloproteinase 17 (ADAM17) is a membrane-bound enzyme reported to mediate SMC hypertrophy through activation of epidermal growth factor receptor (EGFR). We investigated the role of ADAM17 in Ang II-induced hypertension and end-organ damage. VSMC was isolated from mice with intact ADAM17 expression (Adam17(f/f)) or lacking ADAM17 in the SMC (Adam17(f/f)/Cre(Sm22)). Human VSMCs were isolated from the aorta of donors, and ADAM17 deletion was achieved by siRNA transfection...
December 16, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27986445/nadph-oxidase-4-regulates-vascular-inflammation-in-aging-and-atherosclerosis
#13
Andrey Lozhkin, Aleksandr E Vendrov, Hua Pan, Samuel A Wickline, Nageswara R Madamanchi, Marschall S Runge
We recently reported that increased NADPH oxidase 4 (NOX4) expression and activity during aging results in enhanced cellular and mitochondrial oxidative stress, vascular inflammation, dysfunction, and atherosclerosis. The goal of the present study was to elucidate the molecular mechanism(s) for these effects and determine the importance of NOX4 modulation of proinflammatory gene expression in mouse vascular smooth muscle cells (VSMCs). A novel peptide-mediated siRNA transfection approach was used to inhibit Nox4 expression with minimal cellular toxicity...
December 14, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27986444/%C3%AF-3-polyunsaturated-fatty-acids-for-heart-failure-effects-of-dose-on-efficacy-and-novel-signaling-through-free-fatty-acid-receptor-4
#14
REVIEW
Timothy D O'Connell, Robert C Block, Shue P Huang, Gregory C Shearer
Heart failure (HF) affects 5.7 million in the U.S., and despite well-established pharmacologic therapy, the 5-year mortality rate remains near 50%. Furthermore, the mortality rate for HF has not declined in years, highlighting the need for new therapeutic options. Omega-3 polyunsaturated fatty acids (ω3-PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are important regulators of cardiovascular health. However, questions of efficacy and mechanism of action have made the use of ω3-PUFAs in all cardiovascular disease (CVD) controversial...
December 13, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27955979/cardiac-inflammation-in-genetic-dilated-cardiomyopathy-caused-by-mybpc3-mutation
#15
Thomas L Lynch, Mohamed Ameen Ismahil, Anil G Jegga, Michael J Zilliox, Christian Troidl, Sumanth D Prabhu, Sakthivel Sadayappan
Cardiomyopathies are a leading cause of heart failure and are often caused by mutations in sarcomeric genes, resulting in contractile dysfunction and cellular damage. This may stimulate the production of a robust proinflammatory response. To determine whether myocardial inflammation is associated with cardiac dysfunction in dilated cardiomyopathy (DCM) caused by MYBPC3 mutation, we used the well-characterized cMyBP-C((t/t)) mouse model of DCM at 3months of age. Compared to wild type (WT) mice, DCM mice exhibited significantly decreased fractional shortening (36...
December 10, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27914791/aberrant-developmental-titin-splicing-and-dysregulated-sarcomere-length-in-thymosin-%C3%AE-4-knockout-mice
#16
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/27914790/sarcoplasmic-reticulum-ca-2-mg-2-k-and-cl-concentrations-adjust-quickly-as-heart-rate-changes
#17
Claudio Berti, Vilmos Zsolnay, Thomas R Shannon, Michael Fill, Dirk Gillespie
During systole, Ca(2+) is released from the sarcoplasmic reticulum (SR) through ryanodine receptors (RyRs) while, simultaneously, other ions (specifically K(+), Mg(2+), and Cl(-)) provide counter-ion flux. These ions move back into the SR during diastole through the SERCA pump and SR K(+) and Cl(-) channels. In homeostasis, all ion concentrations in different cellular regions (e.g., junctional and non-junctional SR, dyadic cleft, and cytosol) are the same at the beginning and end of the cardiac cycle. Here, we used an equivalent circuit compartment model of the SR and the surrounding cytoplasm to understand the heart rate dependence of SR ion homeostasis...
November 30, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27913284/cardiac-proteasome-functional-insufficiency-plays-a-pathogenic-role-in-diabetic-cardiomyopathy
#18
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 30, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27913283/i-love-it-when-a-plan-comes-together-insight-gained-through-convergence-of-competing-mathematical-models
#19
EDITORIAL
Jingqi Q X Gong, Jaehee V Shim, Elisa Núñez-Acosta, Eric A Sobie
No abstract text is available yet for this article.
November 30, 2016: Journal of Molecular and Cellular Cardiology
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 29, 2016: Journal of Molecular and Cellular Cardiology
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