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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/28214509/haplodeficiency-of-activin-receptor-like-kinase-4-alleviates-myocardial-infarction-induced-cardiac-fibrosis-and-preserves-cardiac-function
#1
Yi-He Chen, Qian Wang, Chang-Yi Li, Jian-Wen Hou, Xiao-Meng Chen, Qing Zhou, Jie Chen, Yue-Peng Wang, Yi-Gang Li
Cardiac fibrosis (CF), a repairing process following myocardial infarction (MI), is characterized by abnormal proliferation of cardiac fibroblasts and excessive deposition of extracellular matrix (ECM) resulting in inevitable resultant heart failure. TGF-β (transforming growth factor-β)/ALK5 (Activin receptor-like kinase 5)/Smad2/3/4 pathways have been reported to be involved in the process. Recent studies have implicated both activin and its specific downstream component ALK4 in stimulating fibrosis in non-cardiac organs...
February 15, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28189650/functional-studies-can-contribute-to-predict-the-pathogenicity-of-a-novel-mutation-for-cardiomyopathy
#2
LETTER
Andreas Brodehl, Hendrik Milting
No abstract text is available yet for this article.
February 8, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28143713/intercellular-transfer-of-mir-126-3p-by-endothelial-microparticles-reduces-vascular-smooth-muscle-cell-proliferation-and-limits-neointima-formation-by-inhibiting-lrp6
#3
Felix Jansen, Tobias Stumpf, Sebastian Proebsting, Bernardo S Franklin, Daniela Wenzel, Philipp Pfeifer, Anna Flender, Theresa Schmitz, Xiaoyan Yang, Bernd K Fleischmann, Georg Nickenig, Nikos Werner
BACKGROUND: Vascular smooth muscle cell (VSMC) proliferation is of importance in the pathogenesis of vascular diseases such as restenosis or atherosclerosis. Endothelial microparticles (EMPs) regulate function and phenotype of target endothelial cells (ECs), but their influence on VSMC biology is unknown. We aim to investigate the role of EMPs in the regulation of vascular smooth muscle cell (VSMC) proliferation and vascular remodeling. METHODS AND RESULTS: Systemic treatment of mice with EMPs after vascular injury reduced neointima formation in vivo...
January 28, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28131631/ryanodine-receptor-modification-and-regulation-by-intracellular-ca-2-and-mg-2-in-healthy-and-failing-human-hearts
#4
K Walweel, P Molenaar, M S Imtiaz, A Denniss, C Dos Remedios, D F van Helden, A F Dulhunty, D R Laver, N A Beard
RATIONALE: Heart failure is a multimodal disorder, of which disrupted Ca(2+) homeostasis is a hallmark. Central to Ca(2+) homeostasis is the major cardiac Ca(2+) release channel - the ryanodine receptor (RyR2) - whose activity is influenced by associated proteins, covalent modification and by Ca(2+) and Mg(2+). That RyR2 is remodelled and its function disturbed in heart failure is well recognized, but poorly understood. OBJECTIVE: To assess Ca(2+) and Mg(2+) regulation of RyR2 from left ventricles of healthy, cystic fibrosis and failing hearts, and to correlate these functional changes with RyR2 modifications and remodelling...
January 25, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28131630/the-effect-of-pka-mediated-phosphorylation-of-ryanodine-receptor-on-sr-ca-2-leak-in-ventricular-myocytes
#5
Elisa Bovo, Sabine Huke, Lothar A Blatter, Aleksey V Zima
Functional impact of cardiac ryanodine receptor (type 2 RyR or RyR2) phosphorylation by protein kinase A (PKA) remains highly controversial. In this study, we characterized a functional link between PKA-mediated RyR2 phosphorylation level and sarcoplasmic reticulum (SR) Ca(2+) release and leak in permeabilized rabbit ventricular myocytes. Changes in cytosolic [Ca(2+)] and intra-SR [Ca(2+)]SR were measured with Fluo-4 and Fluo-5N, respectively. Changes in RyR2 phosphorylation at two PKA sites, serine-2031 and -2809, were measured with phospho-specific antibodies...
January 25, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28130118/targeting-the-pathway-of-gsk-3%C3%AE-nerve-growth-factor-to-attenuate-post-infarction-arrhythmias-by-preconditioned-adipose-derived-stem-cells
#6
Tsung-Ming Lee, Horng-Jyh Harn, Tzyy-Wen Chiou, Ming-Hsi Chuang, Chun-Hung Chen, Po-Cheng Lin, Shinn-Zong Lin
Adipose-derived stem cell (ADSC) transplantation is a promising new therapy to improve cardiac function after myocardial infarction. However, its low efficacy of transdifferentiation hampers its usefulness. Glycogen synthase kinase-3β (GSK-3β) signal has been shown to play a role in preconditioning-induced cardioprotection. We assessed whether n-butylidenephthalide (BP) primed ADSCs can attenuate arrhythmias by a GSK-3β-dependent pathway after myocardial infarction. Male Wistar rats after coronary ligation was randomly allocated to receive intramyocardial injection of vehicle, ADSCs, BP-preconditioned ADSCs, (BP+lithium)-preconditioned ADSCs, (BP+SB216763)-preconditioned ADSCs, and (BP+LY294002)-preconditioned ADSCs...
January 24, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28119060/conditional-knockout-of-fgf13-in-murine-hearts-increases-arrhythmia-susceptibility-and-reveals-novel-ion-channel-modulatory-roles
#7
Xiangchong Wang, He Tang, Eric Q Wei, Zhihua Wang, Jing Yang, Rong Yang, Sheng Wang, Yongjian Zhang, Geoffrey S Pitt, Hailin Zhang, Chuan Wang
The intracellular fibroblast growth factors (iFGF/FHFs) bind directly to cardiac voltage gated Na(+) channels, and modulate their function. Mutations that affect iFGF/FHF-Na(+) channel interaction are associated with arrhythmia syndromes. Although suspected to modulate other ionic currents, such as Ca(2+) channels based on acute knockdown experiments in isolated cardiomyocytes, the in vivo consequences of iFGF/FHF gene ablation on cardiac electrical activity are still unknown. We generated inducible, cardiomyocyte-restricted Fgf13 knockout mice to determine the resultant effects of Fgf13 gene ablation...
January 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28111173/cardiac-expression-of-ryanodine-receptor-subtype-3-a-strategic-component-in-the-intracellular-ca-2-release-system-of-purkinje-fibers-in-large-mammalian-heart
#8
Rebecca E Daniels, Kazi T Haq, Lawson S Miller, Elizabeth W Chia, Masahito Miura, Vincenzo Sorrentino, John J McGuire, Bruno D Stuyvers
BACKGROUND: Three distinct Ca(2+) release channels were identified in dog P-cells: the ryanodine receptor subtype 2 (RyR2) was detected throughout the cell, while the ryanodine receptor subtype 3 (RyR3) and inositol phosphate sensitive Ca(2+) release channel (InsP3R) were found in the cell periphery. How each of these channels contributes to the Ca(2+) cycling of P-cells is unclear. Recent modeling of Ca(2+) mobilization in P-cells suggested that Ca(2+) sensitivity of Ca(2+)induced Ca(2+)release (CICR) was larger at the P-cell periphery...
January 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28109765/response-to-comment-to-the-article-diverse-contribution-of-bone-marrow-derived-late-outgrowth-endothelial-progenitor-cells-to-vascular-repair-under-pulmonary-arterial-hypertension-and-arterial-neointimal-formation
#9
Masayasu Ikutomi, Yoshiyasu Minami, Makoto Sahara
No abstract text is available yet for this article.
January 18, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28108310/autophagic-dysregulation-in-doxorubicin-cardiomyopathy
#10
REVIEW
Jordan J Bartlett, Purvi C Trivedi, Thomas Pulinilkunnil
Doxorubicin (DOX)-induced cardiotoxicity has been a well-known phenomenon to clinicians and scientists for decades; however, molecular mechanisms underlying DOX cardiotoxicity are still being uncovered. Although the majority of prior research have implicated nuclear and mitochondrial events to be an important etiological aspects of DOX cardiomyopathy, recent discoveries in autophagy have highlighted the renewed interest in the role of lysosome in DOX cardiomyopathy. Indeed, dysregulation of lysosomal autophagy is observed in pre-clinical models of DOX cardiotoxicity...
January 17, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28089740/early-remodeling-of-repolarizing-k-currents-in-the-%C3%AE-mhc-403-mouse-model-of-familial-hypertrophic-cardiomyopathy
#11
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 13, 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
#12
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 12, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28087265/myocardial-relaxation-is-accelerated-by-fast-stretch-not-reduced-afterload
#13
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 11, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28077294/into-the-golden-anniversary-of-the-yellow-journal
#14
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
#15
Charles B B Gray, Takeshi Suetomi, Sunny Xiang, Erik A Blackwood, Christopher C Glembotski, Shigeki Miyamoto, B Daan Westenbrink, Shikha Mishra, 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
#16
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
#17
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
#18
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
#19
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
#20
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
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