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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/28322869/scaffold-free-high-throughput-generation-of-quiescent-valvular-microtissues
#1
Annelies Roosens, Inès Puype, Ria Cornelissen
AIMS: The major challenge of working with valvular interstitial cells in vitro is the preservation or recovery of their native quiescent state. In this study, a biomimetic approach is used which aims to engineer small volume, high quality valve microtissues, having a potential in regenerative medicine and as a relevant 3D in vitro model to provide insights into valve (patho)biology. METHODS AND RESULTS: To form micro-aggregates, porcine valvular interstitial cells were seeded in agarose micro-wells and cultured in medium supplemented with 250μM Ascorbic Acid 2-phosphate for 22days...
March 17, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28302382/congenital-heart-defect-causing-mutation-in-nkx2-5-displays-in-vivo-functional-deficit
#2
Abeer F Zakariyah, Rashida F Rajgara, John P Veinot, Ilona S Skerjanc, Patrick G Burgon
The Nkx2.5 gene encodes a transcription factor that plays a critical role in heart development. In humans, heterozygous mutations in NKX2.5 result in congenital heart defects (CHDs). However, the molecular mechanisms by which these mutations cause the disease remain unknown. NKX2.5-R142C is a mutation that was reported to be associated with atrial septal defect (ASD) and atrioventricular (AV) block in 13-patients from one family. The R142C mutation is located within both the DNA-binding domain and the nuclear localization sequence of NKX2...
March 14, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28279663/mir-146a-mediates-inflammatory-changes-and-fibrosis-in-the-heart-in-diabetes
#3
Biao Feng, Shali Chen, Andrew Devon Gordon, Subrata Chakrabarti
Hyperglycemia induced endothelial injury is a key pathogenetic factor in diabetic cardiomyopathy. In diabetes, changes in pro-inflammatory cytokines are a key mechanism leading to cardiac fibrosis. We have previously demonstrated alteration of miR-146a in chronic diabetic complications. Here, we investigated the role of endothelial miR-146a in mediating inflammation and fibrosis in diabetic cardiomyopathy. To examine the effects of miR-146a on the inflammatory mediators, an endothelial specific miR-146a overexpressing transgenic mice (TG) using tie-2 promoter, was generated...
March 6, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28274624/the-apolipoprotein-a-i-mimetic-peptide-d-4f-alleviates-ox-ldl-induced-oxidative-stress-and-promotes-endothelial-repair-through-the-enos-ho-1-pathway
#4
Donghui Liu, Zhenzhen Ding, Mengzhang Wu, Wenqi Xu, Mingming Qian, Qian Du, Le Zhang, Ye Cui, Jianlan Zheng, He Chang, Caihua Huang, Donghai Lin, Yan Wang
Apolipoprotein A-I (apoA-I) mimetic peptide exerts many anti-atherogenic properties. However, the underlying mechanisms related to the endothelial protective effects remain elusive. In this study, the apoA-I mimetic peptide, D-4F, was used. Proliferation assay, wound healing, and transwell migration experiments showed that D-4F improved the impaired endothelial proliferation and migration resulting from ox-LDL. Endothelial adhesion molecules expression and monocyte adhesion assay demonstrated that D-4F inhibited endothelial inflammation...
March 6, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28263756/neuregulin-1%C3%AE-induces-proliferation-survival-and-paracrine-signaling-in-normal-human-cardiac-ventricular-fibroblasts
#5
Annet Kirabo, Sergey Ryzhov, Manisha Gupte, Seng Sengsayadeth, Richard J Gumina, Douglas B Sawyer, Cristi L Galindo
Neuregulin-1β (NRG-1β) is critical for cardiac development and repair, and recombinant forms are currently being assessed as possible therapeutics for systolic heart failure. We previously demonstrated that recombinant NRG-1β reduces cardiac fibrosis in an animal model of cardiac remodeling and heart failure, suggesting that there may be direct effects on cardiac fibroblasts. Here we show that NRG-1β receptors (ErbB2, ErbB3, and ErbB4) are expressed in normal human cardiac ventricular (NHCV) fibroblast cell lines...
March 3, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28257761/membrane-potential-determines-calcium-alternans-through-modulation-of-sr-ca-2-load-and-l-type-ca-2-current
#6
Giedrius Kanaporis, Lothar A Blatter
Alternans is a risk factor for cardiac arrhythmia, including atrial fibrillation. At the cellular level alternans is observed as beat-to-beat alternations in contraction, action potential (AP) morphology and magnitude of the Ca(2+) transient (CaT). It is widely accepted that the bi-directional interplay between membrane voltage and Ca(2+) is crucial for the development of alternans, however recently the attention has shifted to instabilities in cellular Ca(2+) handling, while the role of AP alternation remains poorly understood...
February 28, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28257760/induction-of-mir133a-expression-by-il-19-targets-ldlrap1-and-reduces-oxldl-uptake-in-vsmc
#7
Khatuna Gabunia, Allison B Herman, Mitali Ray, Sheri E Kelemen, Ross N England, Raul DeLa Cadena, William J Foster, Katherine J Elliott, Satoru Eguchi, Michael V Autieri
The transformation of vascular smooth muscle cells [VSMC] into foam cells leading to increased plaque size and decreased stability is a key, yet understudied step in atherogenesis. We reported that Interleukin-19 (IL-19), a novel, anti-inflammatory cytokine, attenuates atherosclerosis by anti-inflammatory effects on VSMC. In this work we report that IL-19 induces expression of miR133a, a muscle-specific miRNA, in VSMC. Although previously unreported, we report that miR133a can target and reduce mRNA abundance, mRNA stability, and protein expression of Low Density Lipoprotein Receptor Adaptor Protein 1, (LDLRAP1), an adaptor protein which functions to internalize the LDL receptor...
February 28, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28232072/brg1-and-brm-function-antagonistically-with-c-myc-in-adult-cardiomyocytes-to-regulate-conduction-and-contractility
#8
Monte S Willis, Darcy Wood Holley, Zhongjing Wang, Xin Chen, Megan Quintana, Brian C Jensen, Manasi Tannu, Joel Parker, Darwin Jeyaraj, Mukesh K Jain, Julie A Wolfram, Hyoung-Gon Lee, Scott J Bultman
RATIONALE: The contractile dysfunction that underlies heart failure involves perturbations in multiple biological processes ranging from metabolism to electrophysiology. Yet the epigenetic mechanisms that are altered in this disease state have not been elucidated. SWI/SNF chromatin-remodeling complexes are plausible candidates based on mouse knockout studies demonstrating a combined requirement for the BRG1 and BRM catalytic subunits in adult cardiomyocytes. Brg1/Brm double mutants exhibit metabolic and mitochondrial defects and are not viable although their cause of death has not been ascertained...
February 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28223222/disrupting-the-key-circadian-regulator-clock-leads-to-age-dependent-cardiovascular-disease
#9
Faisal J Alibhai, Jonathan LaMarre, Cristine J Reitz, Elena V Tsimakouridze, Jeffrey T Kroetsch, Steffen-Sebastian Bolz, Alex Shulman, Samantha Steinberg, Thomas P Burris, Gavin Y Oudit, Tami A Martino
The circadian mechanism underlies daily rhythms in cardiovascular physiology and rhythm disruption is a major risk factor for heart disease and worse outcomes. However, the role of circadian rhythms is generally clinically unappreciated. Clock is a core component of the circadian mechanism and here we examine the role of Clock as a vital determinant of cardiac physiology and pathophysiology in aging. Clock(Δ19/Δ19) mice develop age-dependent increases in heart weight, hypertrophy, dilation, impaired contractility, and reduced myogenic responsiveness...
February 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28223221/the-atheroma-plaque-secretome-stimulates-the-mobilization-of-endothelial-progenitor-cells-ex-vivo
#10
Francisco M Vega, Violette Gautier, Cecilia M Fernandez-Ponce, M J Extremera, A F M Altelaar, Jaime Millan, Juan C Tellez, Jose A Hernandez-Campos, Rosario Conejero, Jorge Bolivar, Ricardo Pardal, Francisco J Garcia-Cózar, Enrique Aguado, Albert J R Heck, Mª Carmen Duran-Ruiz
Endothelial progenitor cells (EPCs) constitute a promising alternative in cardiovascular regenerative medicine due to their assigned role in angiogenesis and vascular repair. In response to injury, EPCs promote vascular remodeling by replacement of damaged endothelial cells and/or by secreting angiogenic factors over the damaged tissue. Nevertheless, such mechanisms need to be further characterized. In the current approach we have evaluated the initial response of early EPCs (eEPCs) from healthy individuals after direct contact with the factors released by carotid arteries complicated with atherosclerotic plaques (AP), in order to understand the mechanisms underlying the neovascularization and remodeling properties assigned to these cells...
February 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28214509/haplodeficiency-of-activin-receptor-like-kinase-4-alleviates-myocardial-infarction-induced-cardiac-fibrosis-and-preserves-cardiac-function
#11
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 16, 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
#12
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
#13
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/28130118/targeting-the-pathway-of-gsk-3%C3%AE-nerve-growth-factor-to-attenuate-post-infarction-arrhythmias-by-preconditioned-adipose-derived-stem-cells
#14
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
#15
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
#16
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/28108310/autophagic-dysregulation-in-doxorubicin-cardiomyopathy
#17
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/28077294/into-the-golden-anniversary-of-the-yellow-journal
#18
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/28131631/ryanodine-receptor-modification-and-regulation-by-intracellular-ca-2-and-mg-2-in-healthy-and-failing-human-hearts
#19
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...
March 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
#20
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...
March 2017: Journal of Molecular and Cellular Cardiology
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