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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/29913136/mmp-2-and-mmp-9-contribute-to-the-angiogenic-effect-produced-by-hypoxia-15-hete-in-pulmonary-endothelial-cells
#1
Ying Liu, Hongyue Zhang, Lixin Yan, Wei Du, Min Zhang, He Chen, Lixin Zhang, Guangqun Li, Jijin Li, Yinchu Dong, Daling Zhu
Matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) are the predominant gelatinases in the developing lung. Studies have shown that the expression of MMP-2 and MMP-9 is upregulated in hypoxic fibroblasts, 15-hydroxyeicosatetraenoic acid (15-HETE) regulated fibroblasts migration via modulating MMP-2 or MMP-9, and that hypoxia/15-HETE is a predominant contributor to the development of pulmonary arterial hypertension (PAH) through increased angiogenesis. However, the roles of MMP-2 and MMP-9 in pulmonary arterial endothelial cells (PAECs) angiogenesis as well as the molecular mechanism of hypoxia-regulated MMP-2 and MMP-9 expression have not been identified...
June 15, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29908919/frank-s-law-of-the-heart-found-in-translation
#2
EDITORIAL
Pieter P de Tombe, John V Tyberg
No abstract text is available yet for this article.
June 14, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29907408/corrigendum-to-impaired-ca-2-cycling-of-nonischemic-myocytes-contributes-to-sarcomere-dysfunction-early-after-myocardial-infarction-j-mol-cell-cardiol-119-2018-28-39
#3
Annette Kronenbitter, Florian Funk, Katarzyna Hackert, Simone Gorreßen, Dennis Glaser, Peter Boknik, Gereon Poschmann, Kai Stühler, Malgorzata Isić, Martina Krüger, Joachim P Schmitt
No abstract text is available yet for this article.
June 12, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29885959/increased-right-atrial-appendage-apoptosis-is-associated-with-differential-regulation-of-candidate-micrornas-1-and-133a-in-patients-who-developed-atrial-fibrillation-after-cardiac-surgery
#4
James N Tsoporis, Anastasia Fazio, Ioannis K Rizos, Shehla Izhar, Gerald Proteau, Vasileos Salpeas, Angelos Rigopoulos, Eleftarios Sakadakis, Ioannis K Toumpoulis, Thomas G Parker
Atrial fibrillation (AF) following on-pump coronary artery bypass grafting (CABG) is a common condition associated with increased morbidity and mortality. We investigated the possibility that miRs may play a contributory role in postoperative AF and associated apoptosis. A total of 42 patients (31 males and 11 females, mean age 65.0 ± 1.3 years) with sinus rhythm and without a history of AF were prospectively enrolled. We examined the levels of the muscle-specific miRs 1 and 133A and markers of apoptosis including TUNEL staining, caspase-3 activation, Bcl2 and Bax mRNAs in right atrial appendage (RAA) biopsies and blood plasma taken before aortic cross-clamping and after reperfusion...
June 7, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29885334/compartmentalized-cyclic-nucleotides-have-opposing-effects-on-regulation-of-hypertrophic-phospholipase-c%C3%AE%C2%B5-signaling-in-cardiac-myocytes
#5
Craig A Nash, Loren M Brown, Sundeep Malik, Xiaodong Cheng, Alan V Smrcka
In cardiac myocytes activation of an exchange factor activated by cAMP (Epac) leads to activation of phospholipase Cε (PLCε)-dependent hydrolysis of phosphatidylinositol 4-phosphate (PI4P) in the Golgi apparatus a process critical for development of cardiac hypertrophy. Here we show that β-adrenergic receptor (βAR) stimulation does not stimulate this pathway in the presence of the broad spectrum phosphodiesterase (PDE) inhibitor IBMX, but selective PDE3 inhibition revealed βAR-dependent PI4P depletion...
June 6, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29879406/the-protective-role-of-toll-like-receptor-3-and-type-i-interferons-in-the-pathophysiology-of-vein-graft-disease
#6
K H Simons, M R de Vries, H A B Peters, J F Hamming, J W Jukema, P H A Quax
BACKGROUND: Venous grafts are commonly used as conduits to bypass occluded arteries. Unfortunately, patency rates are limited by vein graft disease (VGD). Toll like receptors (TLRs) can be activated in vein grafts by endogenous ligands. This study aims to investigate the role of TLR3 in VGD. METHODS: Vein graft surgery was performed by donor caval vein interpositioning in the carotid artery of recipient Tlr2-/- , Tlr3-/- , Tlr4-/- and control mice. Vein grafts were harvested 7, 14 and 28d after surgery to perform immunohistochemical analysis...
June 4, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29807024/beta1-adrenoceptor-antagonist-metoprolol-attenuates-cardiac-myocyte-ca-2-handling-dysfunction-in-rats-with-pulmonary-artery-hypertension
#7
Ewan D Fowler, Mark J Drinkhill, Ruth Norman, Eleftheria Pervolaraki, Rachel Stones, Emma Steer, David Benoist, Derek S Steele, Sarah C Calaghan, Ed White
Right heart failure is the major cause of death in Pulmonary Artery Hypertension (PAH) patients but is not a current, specific therapeutic target. Pre-clinical studies have shown that adrenoceptor blockade can improve cardiac function but the mechanisms of action within right ventricular (RV) myocytes are unknown. We tested whether the β1 -adrenoceptor blocker metoprolol could improve RV myocyte function in an animal model of PAH, by attenuating adverse excitation-contraction coupling remodeling. PAH with RV failure was induced in rats by monocrotaline injection...
May 26, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29800555/a-novel-adenylyl-cyclase-type-5-inhibitor-that-reduces-myocardial-infarct-size-even-when-administered-after-coronary-artery-reperfusion
#8
Jie Zhang, Daniel Levy, Marko Oydanich, Claudio A Bravo, Seonghun Yoon, Dorothy E Vatner, Stephen F Vatner
We developed a novel adenylyl cyclase type 5 (AC5) inhibitor, C90, that reduces myocardial infarct size even when administered after coronary reperfusion. This is key, since it is not practical to administer a drug to a patient with myocardial infarction before revascularization, and is one reason why so many prior drugs, which reduced infarct in experimental animals, failed in clinical trials. C90 is the most potent AC5 inhibitor, as exhibited by its IC50 value for AC5 inhibition, which was 5 times lower than the next most potent AC5 inhibitor...
May 22, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29800554/repressive-histone-methylation-regulates-cardiac-myocyte-cell-cycle-exit
#9
Danny El-Nachef, Kyohei Oyama, Yun-Yu Wu, Miles Freeman, Yiqiang Zhang, W Robb MacLellan
Mammalian cardiac myocytes (CMs) stop proliferating soon after birth and subsequent heart growth comes from hypertrophy, limiting the adult heart's regenerative potential after injury. The molecular events that mediate CM cell cycle exit are poorly understood. To determine the epigenetic mechanisms limiting CM cycling in adult CMs (ACMs) and whether trimethylation of lysine 9 of histone H3 (H3K9me3), a histone modification associated with repressed chromatin, is required for the silencing of cell cycle genes, we developed a transgenic mouse model where H3K9me3 is specifically removed in CMs by overexpression of histone demethylase, KDM4D...
May 22, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29793733/corrigendum-to-interactive-effect-of-beta-adrenergic-stimulation-and-mechanical-stretch-on-low-frequency-oscillations-of-ventricular-action-potential-duration-in-humans-j-mol-cell-cardiol-97-2016-93-105
#10
Esther Pueyo, Michele Orini, José F Rodríguez, Peter Taggart
No abstract text is available yet for this article.
May 21, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29792884/pharmacological-inhibition-of-dna-methylation-attenuates-pressure-overload-induced-cardiac-hypertrophy-in-rats
#11
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/29778253/corrigendum-to-endothelial-nitric-oxide-signaling-regulates-notch1-in-aortic-valve-disease-j-mol-cell-cardiol-60-2013-27-35
#12
K Bosse, C P Hans, N Zhao, S N Koenig, N Huang, A Guggilam, S LaHaye, G Tao, P A Lucchesi, J Lincoln, B Lilly, V Garg
No abstract text is available yet for this article.
May 16, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29777691/improving-electrical-properties-of-ipsc-cardiomyocytes-by-enhancing-cx43-expression
#13
Valentin Sottas, Carl-Mattheis Wahl, Mihnea C Trache, Michael Bartolf-Kopp, Sidney Cambridge, Markus Hecker, Nina D Ullrich
The therapeutic potential of induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) is limited by immature functional features including low impulse propagation and reduced cell excitability. Key players regulating electrical activity are voltage-gated Na+ channels (Nav 1.5) and gap junctions built from connexin-43 (Cx43). Here we tested the hypothesis that enhanced Cx43 expression increases intercellular coupling and influences excitability by modulating Nav 1.5. Using transgenic approaches, Cx43 and Nav 1...
May 16, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29777690/adjusted-analysis
#14
Paul Lee
No abstract text is available yet for this article.
May 16, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29758225/trpv6-protects-er-stress-induced-apoptosis-via-atf6%C3%AE-trpv6-jnk-pathway-in-human-embryonic-stem-cell-derived-cardiomyocytes
#15
Zhichao Li, Zhaoyue Meng, Jun Lu, Francis M Chen, Wing-Tak Wong, Gary Tse, Changbo Zheng, Wendy Keung, Kennis Tse, Ronald A Li, Liwen Jiang, Xiaoqiang Yao
Human pluripotent stem cell-derived cardiomyocytes have potential applications in disease modeling and drug screening. Therefore, it is important to understand the mechanisms and signaling pathways underlying the survival and death of these cells. Endoplasmic reticulum (ER) stress is triggered by various cellular stresses that disturb protein folding in the ER. Cells cope with ER stress by activating the unfolded protein response (UPR), a homeostatic signaling network that orchestrates the recovery of ER function...
May 16, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29775643/myocardial-infarction-induced-hippocampal-microtubule-damage-by-cardiac-originating-microrna-1-in-mice
#16
Lin-Lin Sun, Ming-Jing Duan, Ji-Chao Ma, Ling Xu, Meng Mao, Das Biddyut, Qin Wang, Chao Yang, Shuai Zhang, Yi Xu, Lin Yang, You Tian, Ying Liu, Sheng-Nan Xia, Ke-Xin Li, Zhuo Jin, Qiaojie Xiong, Jing Ai
Cardiovascular diseases are risk factors for dementia, but the mechanisms remain elusive. Here, we report that myocardial infarction (MI) generated by the ligation of the left coronary artery (LCA) could lead to increased miR-1 levels in the hippocampus and blood with neuronal microtubule damage and decreased TPPP/p25 protein expression in the hippocampus. These changes could be prevented by a knockdown of miR-1 using hippocampal stereotaxic injections of anti-miR-1 oligonucleotide fragments carried by a lentivirus vector (lenti-pre-AMO-miR-1)...
May 15, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29752948/functional-and-transcriptomic-insights-into-pathogenesis-of-r9c-phospholamban-mutation-using-human-induced-pluripotent-stem-cell-derived-cardiomyocytes
#17
Delaine K Ceholski, Irene C Turnbull, Chi-Wing Kong, Simon Koplev, Joshua Mayourian, Przemek A Gorski, Francesca Stillitano, Angelos A Skodras, Mathieu Nonnenmacher, Ninette Cohen, Johan L M Björkegren, Daniel R Stroik, Razvan L Cornea, David D Thomas, Ronald A Li, Kevin D Costa, Roger J Hajjar
Dilated cardiomyopathy (DCM) can be caused by mutations in the cardiac protein phospholamban (PLN). We used CRISPR/Cas9 to insert the R9C PLN mutation at its endogenous locus into a human induced pluripotent stem cell (hiPSC) line from an individual with no cardiovascular disease. R9C PLN hiPSC-CMs display a blunted β-agonist response and defective calcium handling. In 3D human engineered cardiac tissues (hECTs), a blunted lusitropic response to β-adrenergic stimulation was observed with R9C PLN. hiPSC-CMs harboring the R9C PLN mutation showed activation of a hypertrophic phenotype, as evidenced by expression of hypertrophic markers and increased cell size and capacitance of cardiomyocytes...
May 9, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29750994/regulation-of-cardiac-fibroblast-mmp2-gene-expression-by-scleraxis
#18
Raghu S Nagalingam, Hamza A Safi, Danah S Al-Hattab, Rushita A Bagchi, Natalie M Landry, Ian M C Dixon, Jeffrey T Wigle, Michael P Czubryt
Remodeling of the cardiac extracellular matrix is responsible for a number of the detrimental effects on heart function that arise secondary to hypertension, diabetes and myocardial infarction. This remodeling consists both of an increase in new matrix protein synthesis, and an increase in the expression of matrix metalloproteinases (MMPs) that degrade existing matrix structures. Previous studies utilizing knockout mice have demonstrated clearly that MMP2 plays a pathogenic role during matrix remodeling, thus it is important to understand the mechanisms that regulate MMP2 gene expression...
May 8, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29750993/mutation-of-the-na-k-atpase-atp1a1a-1-causes-qt-interval-prolongation-and-bradycardia-in-zebrafish
#19
Alexander Pott, Sarah Bock, Ina M Berger, Karen Frese, Tillman Dahme, Mirjam Kessler, Susanne Rinné, Niels Decher, Steffen Just, Wolfgang Rottbauer
The genetic underpinnings that orchestrate the vertebrate heart rate are not fully understood yet, but of high clinical importance, since diseases of cardiac impulse formation and propagation are common and severe human arrhythmias. To identify novel regulators of the vertebrate heart rate, we deciphered the pathogenesis of the bradycardia in the homozygous zebrafish mutant hiphop (hip) and identified a missense-mutation (N851K) in Na+ /K+ -ATPase α1-subunit (atp1a1a.1). N851K affects zebrafish Na+ /K+ -ATPase ion transport capacity, as revealed by in vitro pump current measurements...
May 8, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29746849/characterisation-of-re-entrant-circuit-or-rotational-activity-in-vitro-using-the-hl1-6-myocyte-cell-line
#20
Charles Houston, Konstantinos N Tzortzis, Caroline Roney, Andrea Saglietto, David S Pitcher, Chris Cantwell, Rasheda A Chowdhury, Fu Siong Ng, Nicholas S Peters, Emmanuel Dupont
Fibrillation is the most common arrhythmia observed in clinical practice. Understanding of the mechanisms underlying its initiation and maintenance remains incomplete. Functional re-entries are potential drivers of the arrhythmia. Two main concepts are still debated, the "leading circle" and the "spiral wave or rotor" theories. The homogeneous subclone of the HL1 atrial-derived cardiomyocyte cell line, HL1-6, spontaneously exhibits re-entry on a microscopic scale due to its slow conduction velocity and the presence of triggers, making it possible to examine re-entry at the cellular level...
May 7, 2018: Journal of Molecular and Cellular Cardiology
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