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Journal of Molecular and Cellular Cardiology

Xiangbo Gou, Wenying Wang, Sihao Zou, Yajuan Qi, Yanfang Xu
The slowly activating delayed rectifier K+ current (IKs ) is one of the main repolarizing currents in the human heart. Evidence has shown that angiotensin II (Ang II) regulates IKs through the protein kinase C (PKC) pathway, but the related results are controversial. This study was designed to identify PKC isoenzymes involved in the regulation of IKs by Ang II and the underlying molecular mechanism. The whole-cell patch-clamp technique was used to record IKs in isolated guinea pig ventricular cardiomyocytes and in human embryonic kidney (HEK) 293 cells co-transfected with human KCNQ1/KCNE1 genes and Ang II type 1 receptor genes...
February 13, 2018: Journal of Molecular and Cellular Cardiology
Thomas Kampourakis, Saraswathi Ponnam, Malcolm Irving
Hypertrophic cardiomyopathy (HCM) is frequently linked to mutations in the protein components of the myosin-containing thick filaments leading to contractile dysfunction and ultimately heart failure. However, the molecular structure-function relationships that underlie these pathological effects remain largely obscure. Here we chose an example mutation (R58Q) in the myosin regulatory light chain (RLC) that is associated with a severe HCM phenotype and combined the results from a wide range of in vitro and in situ structural and functional studies on isolated protein components, myofibrils and ventricular trabeculae to create an extensive map of structure-function relationships...
February 13, 2018: Journal of Molecular and Cellular Cardiology
Yongkun Zhan, Xiaolei Sun, Bin Li, Huanhuan Cai, Chen Xu, Qianqian Liang, Chao Lu, Ruizhe Qian, Sifeng Chen, Lianhua Yin, Wei Sheng, Guoying Huang, Aijun Sun, Junbo Ge, Ning Sun
PRKAG2 cardiac syndrome is a distinct form of human cardiomyopathy characterized by cardiac hypertrophy, ventricular pre-excitation and progressive cardiac conduction disorder. However, it remains unclear how mutations in the PRKAG2 gene give rise to such a complicated disease. To investigate the underlying molecular mechanisms, we generated disease-specific hiPSC-derived cardiomyocytes from two brothers both carrying a heterozygous missense mutation c.905G>A (R302Q) in the PRKAG2 gene and further corrected the R302Q mutation with CRISPR-Cas9 mediated genome editing...
February 13, 2018: Journal of Molecular and Cellular Cardiology
Rita Carmona, Laura Ariza, Ana Cañete, Ramón Muñoz-Chápuli
The vertebrate heart receives the blood through the cardiac inflow tract. This area has experienced profound changes along the evolution of vertebrates; changes that have a reflection in the cardiac ontogeny. The development of the inflow tract involves dynamic changes due to the progressive addition of tissue derived from the secondary heart field. The inflow tract is the site where oxygenated blood coming from lungs is received separately from the systemic return, where the cardiac pacemaker is established and where the proepicardium develops...
February 13, 2018: Journal of Molecular and Cellular Cardiology
Cheng-Lin Zhang, Qian Zhao, Hui Liang, Xue Qiao, Jin-Yu Wang, Dan Wu, Li-Ling Wu, Li Li
Cardiac fibrosis is characterized by excessive deposition of extracellular matrix (ECM) proteins in the myocardium and results in decreased ventricular compliance and diastolic dysfunction. Cartilage intermediate layer protein-1 (CILP-1), a novel identified cardiac matricellular protein, is upregulated in most conditions associated with cardiac remodeling, however, whether CILP-1 is involved in pressure overload-induced fibrotic response is unknown. Here, we investigated whether CILP-1 was critically involved in the fibrotic remodeling induced by pressure overload...
February 10, 2018: Journal of Molecular and Cellular Cardiology
Qiongqiong Zhou, Xiaogang Peng, Xiao Liu, Leifeng Chen, Qinmei Xiong, Yang Shen, Jinyan Xie, Zhenyan Xu, Lin Huang, Jinzhu Hu, Rong Wan, Kui Hong
FAT10, a member of the ubiquitin-like-modifier family of proteins, plays a cardioprotective role in response to hypoxic/ischemic injury. Caveolin-3 (Cav-3), a muscle-specific caveolin family member, is involved in cardiomyocyte apoptosis. However, the link between FAT10 and Cav-3 in ischemic cardiomyocytes is unclear. In the present study, we found that both FAT10 and Cav-3 were upregulated in ischemic myocardial tissues and in hypoxic cardiomyocytes. Furthermore, our results demonstrated that FAT10 inhibits hypoxia-induced cardiomyocyte apoptosis by increasing Cav-3 expression...
February 10, 2018: Journal of Molecular and Cellular Cardiology
Amanda Soler, Ian Hunter, Gregory Joseph, Rebecca Hutcheson, Brenda Hutcheson, Jenny Yang, Frank Fan Zhang, Sachindra Raj Joshi, Chastity Bradford, Katherine H Gotlinger, Rachana Maniyar, John R Falck, Spencer Proctor, Michal Laniado Schwartzman, Sachin A Gupte, Petra Rocic
Arterial stiffness plays a causal role in development of systolic hypertension. 20-hydroxyeicosatetraeonic acid (20-HETE), a cytochrome P450 (CYP450)-derived arachidonic acid metabolite, is known to be elevated in resistance arteries in hypertensive animal models and loosely associated with obesity in humans. However, the role of 20-HETE in the regulation of large artery remodeling in metabolic syndrome has not been investigated. We hypothesized that elevated 20-HETE in metabolic syndrome increases matrix metalloproteinase 12 (MMP12) activation leading to increased degradation of elastin, increased large artery stiffness and increased systolic blood pressure...
February 8, 2018: Journal of Molecular and Cellular Cardiology
Hong Zhu, Aijun Sun
Programmed cell death plays an essential role in myocardial homeostasis and pathology. Three distinct forms of programmed cell death have been identified, namely apoptosis, necrosis, and autophagic cell death. Necrosis, previously known as an unregulated form of cell death, has been recognized as a highly regulated process now and attracted great attention over the past decade. Programmed necrosis mainly refers to necroptosis, pyroptosis, ferroptosis, and mitochondrial permeability transition (MPT)-dependent necrosis...
February 6, 2018: Journal of Molecular and Cellular Cardiology
Tal Golan-Lagziel, Yair E Lewis, Omer Shkedi, Guy Douvdevany, Lilac H Caspi, Izhak Kehat
Cardiac fibroblasts play key roles in both health and disease. Their regulatory elements, transcription factors (TFs), and mechanisms of expression control have not been fully elucidated. We used a differential open chromatin approach, coupled with active enhancer mark, transcriptomic, and computational TFs binding analysis to map cell-type-specific active enhancers in cardiac fibroblasts and cardiomyocytes, and outline the TFs families that control them. This approach was validated by its ability to uncover the known cardiomyocyte TF biology in an unbiased manner, and was then applied to cardiac fibroblasts...
February 5, 2018: Journal of Molecular and Cellular Cardiology
Julian Mustroph, Olivia Wagemann, Simon Lebek, Daniel Tarnowski, Jasmin Ackermann, Marzena Drzymalski, Steffen Pabel, Christof Schmid, Stefan Wagner, Samuel Sossalla, Lars S Maier, Stefan Neef
AIMS: Ethanol has acute negative inotropic and arrhythmogenic effects. The underlying mechanisms, however, are largely unknown. Sarcoplasmic reticulum Ca2+-leak is an important mechanism for reduced contractility and arrhythmias. Ca2+-leak can be induced by oxidative stress and Ca2+/Calmodulin-dependent protein kinase II (CaMKII). Therefore, we investigated the influence of acute ethanol exposure on excitation-contraction coupling in atrial and ventricular cardiomyocytes. METHODS AND RESULTS: Isolated human atrial and murine atrial or ventricular cardiomyocytes were preincubated for 30 min and then superfused with control solution or solution containing ethanol...
February 2, 2018: Journal of Molecular and Cellular Cardiology
James Winter, Michael Tipton, Michael J Shattock
This study tested the hypothesis that concomitant sympathetic and parasympathetic stimulation ("autonomic conflict") may act as a trigger for arrhythmia in long QT syndrome (LQTS). Studies were performed in isolated innervated rabbit hearts treated with clofilium (100 nmol/L); a potassium channel blocker. The influence of vagus nerve stimulation (VNS) on spontaneous ventricular arrhythmia was assessed in the absence/presence of sustained noradrenaline perfusion (100 nmol/L) and with sudden adrenergic stress (injections of noradrenaline into the perfusion line)...
February 2, 2018: Journal of Molecular and Cellular Cardiology
Pedro Molina-Sánchez, Lara Del Campo, Vanesa Esteban, Cristina Rius, Raphael Chèvre, José J Fuster, Mercedes Ferrer, Juan Miguel Redondo, Vicente Andrés
Phosphorylation at serine 10 (S10) is the major posttranslational modification of the tumor suppressor p27, and is reduced in both human and mouse atherosclerosis. Moreover, a lack of p27-phospho-S10 in apolipoprotein E-null mice (apoE-/-) leads to increased high-fat diet-induced atherosclerosis associated with endothelial dysfunction and augmented leukocyte recruitment. In this study, we analyzed whether p27-phospho-S10 modulates additional endothelial functions and associated pathologies. Defective p27-phospho-S10 increases COX-2 activity in mouse aortic endothelial cells without affecting other key regulators of vascular reactivity, reduces endothelium-dependent dilation, and increases arterial contractility...
February 2, 2018: Journal of Molecular and Cellular Cardiology
Ivan Luptak, Aaron L Sverdlov, Marcello Panagia, Fuzhong Qin, David R Pimentel, Dominique Croteau, Deborah A Siwik, Joanne S Ingwall, Markus M Bachschmid, James A Balschi, Wilson S Colucci
Metabolic syndrome is a cluster of obesity-related metabolic abnormalities that lead to metabolic heart disease (MHD) with left ventricular pump dysfunction. Although MHD is thought to be associated with myocardial energetic deficiency, two key questions have not been answered. First, it is not known whether there is a sufficient energy deficit to contribute to pump dysfunction. Second, the basis for the energy deficit is not clear. To address these questions, mice were fed a high fat, high sucrose (HFHS) 'Western' diet to recapitulate the MHD phenotype...
January 31, 2018: Journal of Molecular and Cellular Cardiology
Ivana Josipovic, Beatrice Pflüger, Christian Fork, Andrea E Vasconez, James A Oo, Juliane Hitzel, Sandra Seredinski, Elisabetta Gamen, Dagmar Meyer Zu Heringdorf, Wei Chen, Mario Looso, Soni Savai Pullamsetti, Ralf P Brandes, Matthias S Leisegang
Sphingosine-1-Phosphate (S1P) is a potent signaling lipid. The effects of S1P are mediated by the five S1P receptors (S1PR). In the endothelium S1PR1 is the predominant receptor and thus S1PR1 abundance limits S1P signaling. Recently, lncRNAs were identified as a novel class of molecules regulating gene expression. Interestingly, the lncRNA NONHSAT004848 (LISPR1, Long intergenic noncoding RNA antisense to S1PR1), is closely positioned to the S1P1 receptors gene and in part shares its promoter region. We hypothesize that LISPR1 controls endothelial S1PR1 expression and thus S1P-induced signaling in endothelial cells...
January 31, 2018: Journal of Molecular and Cellular Cardiology
Xiaowei Nie, Jianxin Tan, Youai Dai, Yun Liu, Jian Zou, Jie Sun, Shugao Ye, Chenyou Shen, Li Fan, Jingyu Chen, Jin-Song Bian
Pulmonary arterial hypertension (PAH) is a devastating cardiopulmonary disorder characterized by pulmonary arterial remodeling mainly due to excess cellular proliferation and apoptosis resistance of pulmonary arterial smooth muscle cells (PASMCs). Reduced bone morphogenetic protein receptor 2 (BMPR2) expression in patients with PAH impairs pulmonary arterial endothelial cells (PAECs) function. This can adversely affect PAEC survival and promote PASMCs proliferation. We hypothesized that interventions to normalize the expression of genes that are targets of the BMPR2 signaling could restore PAECs function and prevent or reverse PAH...
January 31, 2018: Journal of Molecular and Cellular Cardiology
Yuuki Shimizu, Rohini Polavarapu, Kattri-Liis Eskla, Chad K Nicholson, Christopher A Koczor, Rui Wang, William Lewis, Sruti Shiva, David J Lefer, John W Calvert
BACKGROUND: Hydrogen sulfide (H2S) is an important regulator of mitochondrial bioenergetics, but its role in regulating mitochondrial biogenesis is not well understood. Using both genetic and pharmacological approaches, we sought to determine if H2S levels directly influenced cardiac mitochondrial content. RESULTS: Mice deficient in the H2S-producing enzyme, cystathionine γ-lyase (CSE KO) displayed diminished cardiac mitochondrial content when compared to wild-type hearts...
January 29, 2018: Journal of Molecular and Cellular Cardiology
Kai Guo, Lu Hu, Dan Xi, Jinzhen Zhao, Jichen Liu, Tiantian Luo, Yusheng Ma, Wenyan Lai, Zhigang Guo
AIMS: Human genome-wide association studies (GWAS) have found that proline/serine-rich coiled-coil 1 (PSRC1) encodes a protein that is associated with serum lipid levels and coronary artery disease. In addition, our previous study showed that the cholesterol efflux capacity is decreased in macrophages following a treatment silencing Psrc1, indicating that PSRC1 has anti-atherosclerotic effects. However, the role of PSRC1 in the development of atherosclerosis is unknown. This study aims to explore the effect of PSRC1 on atherosclerosis and its underlying mechanisms...
January 25, 2018: Journal of Molecular and Cellular Cardiology
Yair E Lewis, Anner Moskovitz, Michael Mutlak, Joerg Heineke, Lilac H Caspi, Izhak Kehat
The mechanisms responsible for maintaining macromolecular protein complexes, with their proper localization and subunit stoichiometry, are incompletely understood. Here we studied the maintenance of the sarcomere, the basic contractile macromolecular complex of cardiomyocytes. We performed single-cell analysis of cardiomyocytes using imaging of mRNA and protein synthesis, and demonstrate that three distinct mechanisms are responsible for the maintenance of the sarcomere: mRNAs encoding for sarcomeric proteins are localized to the sarcomere, ribosomes are localized to the sarcomere with localized sarcomeric protein translation, and finally, a localized E3 ubiquitin ligase allow efficient degradation of excess unincorporated sarcomeric proteins...
January 22, 2018: Journal of Molecular and Cellular Cardiology
Matheus A Costa, Ana E Paiva, Julia P Andreotti, Marcus V Cardoso, Carlos D Cardoso, Akiva Mintz, Alexander Birbrair
No-reflow phenomenon is defined as the reduced blood flow after myocardial ischemia. If prolonged it leads to profound damages in the myocardium. The lack of a detailed knowledge about the cells mediating no-reflow restricts the design of effective therapies. Recently, O'Farrell et al. (2017) by using state-of-the-art technologies, including high-resolution confocal imaging in combination with myocardial ischemia/reperfusion mouse model, reveal that pericytes contribute to the no-reflow phenomenon post-ischemia in the heart...
January 22, 2018: Journal of Molecular and Cellular Cardiology
Peili Li, Yasutaka Kurata, Mahati Endang, Haruaki Ninomiya, Katsumi Higaki, Fikri Taufiq, Kumi Morikawa, Yasuaki Shirayoshi, Minoru Horie, Ichiro Hisatome
The human ether-a-go-go-related gene (hERG) encodes the α subunit of a rapidly activating delayed-rectifier potassium (IKr) channel. Mutations of the hERG cause long QT syndrome type 2 (LQT2). Acetylation of lysine residues occurs in a subset of non-histone proteins and this modification is controlled by both histone acetyltransferases and deacetylases (HDACs). The aim of this study was to clarify effects of HDAC(s) on wild-type (WT) and mutant hERG proteins. WThERG and two trafficking-defective mutants (G601S and R752W) were transiently expressed in HEK293 cells, which were treated with a pan-HDAC inhibitor Trichostatin A (TSA) or an isoform-selective HDAC6 inhibitor Tubastatin A (TBA)...
January 16, 2018: Journal of Molecular and Cellular Cardiology
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