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Journal of Molecular and Cellular Cardiology

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https://www.readbyqxmd.com/read/29224834/hdac1-localizes-to-the-mitochondria-of-cardiac-myocytes-and-contributes-to-early-cardiac-reperfusion-injury
#1
Daniel J Herr, Mauhamad Baarine, Sverre E Aune, Xiaoyang Li, Lauren E Ball, John J Lemasters, Craig C Beeson, James C Chou, Donald R Menick
RATIONALE: Recent evidence indicates that histone deacetylase enzymes (HDACs) contribute to ischemia reperfusion (I/R) injury, and pan-HDAC inhibitors have been shown to be cardioprotective when administered either before an ischemic insult or during reperfusion. We have shown previously that selective inhibition of class I HDACs provides superior cardioprotection when compared to pan-HDAC inhibition in a pretreatment model, but selective class I HDAC inhibition has not been tested during reperfusion, and specific targets of class I HDACs in I/R injury have not been identified...
December 7, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29217433/hypertrophic-cardiomyopathy-linked-mutation-in-troponin-t-causes-myofibrillar-disarray-and-pro-arrhythmic-action-potential-changes-in-human-ipsc-cardiomyocytes
#2
Lili Wang, Kyungsoo Kim, Shan Parikh, Adrian Gabriel Cadar, Kevin R Bersell, Huan He, Jose R Pinto, Dmytro O Kryshtal, Bjorn C Knollmann
BACKGROUND: Mutations in cardiac troponin T (TnT) are linked to increased risk of ventricular arrhythmia and sudden death despite causing little to no cardiac hypertrophy. Studies in mice suggest that the hypertrophic cardiomyopathy (HCM)-associated TnT-I79N mutation increases myofilament Ca sensitivity and is arrhythmogenic, but whether findings from mice translate to human cardiomyocyte electrophysiology is not known. OBJECTIVES: To study the effects of the TnT-I79N mutation in human cardiomyocytes...
December 4, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29217432/transverse-tubular-network-structures-in-the-genesis-of-intracellular-calcium-alternans-and-triggered-activity-in-cardiac-cells
#3
Zhen Song, Michael B Liu, Zhilin Qu
RATIONALE: The major role of a transverse-tubular (TT) network in a cardiac cell is to facilitate effective excitation-contraction coupling and signaling. The TT network structures are heterogeneous within a single cell, and vary between different types of cells and species. They are also remodeled in cardiac diseases. However, how different TT network structures predispose cardiac cells to arrhythmogenesis remains to be revealed. OBJECTIVE: To systematically investigate the roles of TT network structure and the underlying mechanisms in the genesis of intracellular calcium (Ca2+) alternans and triggered activity (TA)...
December 4, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29217431/the-effects-of-load-on-transmural-differences-in-contraction-of-isolated-mouse-ventricular-cardiomyocytes
#4
Anastasia Khokhlova, Gentaro Iribe, Leonid Katsnelson, Keiji Naruse, Olga Solovyova
Mechanical properties of cardiomyocytes from different transmural regions are heterogeneous in the left ventricular wall. The cardiomyocyte mechanical environment affects this heterogeneity because of mechano-electric feedback mechanisms. In the present study, we investigated the effects of the mechanical load (preload and afterload) on transmural differences in contraction of subendocardial (ENDO) and subepicardial (EPI) single cells isolated from the murine left ventricle. Various preloads imposed via axial stretch and afterloads (unloaded and heavy loaded conditions) were applied to the cells using carbon fiber techniques for single myocytes...
December 4, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29196099/dkk3-overexpression-attenuates-cardiac-hypertrophy-and-fibrosis-in-an-angiotensin-perfused-animal-model-by-regulating-the-adam17-ace2-and-gsk-3%C3%AE-%C3%AE-catenin-pathways
#5
Chun-Gang Zhai, Ye-Yang Xu, Yuan-Yuan Tie, Ya Zhang, Wen-Qiang Chen, Xiao-Ping Ji, Yang Mao, Lei Qiao, Jing Cheng, Qing-Bo Xu, Cheng Zhang
AIMS: Cardiac pressure and humoral factors induce cardiac hypertrophy and fibrosis, which are characterized by increased stiffness, reduced contractility and altered perfusion. Angiotensin II (AngII) is well known to promote this pathology. Angiotensin-converting enzyme (ACE) 2, which cleaves AngII and forms Ang-(1-7), exerts protective anti-hypertrophy and anti-fibrosis effects. A disintegrin and metalloproteinase 17 (ADAM17), a membrane-bound enzyme reported to cleave ACE2, may participate in the pathological process of AngII perfusion-induced heart damage...
December 4, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29197521/high-phosphate-induced-downregulation-of-ppar%C3%AE-contributes-to-ckd-associated-vascular-calcification
#6
Liang Liu, Yong Liu, Ying Zhang, Xianjin Bi, Ling Nie, Chi Liu, Jiachuan Xiong, Ting He, Xinlin Xu, Yanlin Yu, Ke Yang, Jun Gu, Yunjian Huang, Jingbo Zhang, Zhiren Zhang, Bo Zhang, Jinghong Zhao
Medial arterial calcification associated with hyperphosphatemia is a main cause of cardiovascular mortality in patients with chronic kidney disease (CKD), but the mechanisms underlying high phosphate-induced vascular calcification remain largely unknown. Here, we observed a significant decrease in the expression of peroxisome proliferator-activated receptor-gamma (PPARγ) in calcified arteries both in CKD patients and in a mouse model of CKD with hyperphosphatemia. In vitro, high phosphate treatment led to a decreased expression of PPARγ in mouse vascular smooth muscle cells (VMSCs), accompanied by apparent osteogenic differentiation and calcification...
November 29, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29191788/progressive-impairment-of-atrial-myocyte-function-during-left-ventricular-hypertrophy-and-heart-failure
#7
Florentina Pluteanu, Yulia Nikonova, Anna Holzapfel, Birgit Herzog, Anna Scherer, Judit Preisenberger, Jelena Plačkić, Katharina Scheer, Teodora Ivanova, Alicja Bukowska, Andreas Goette, Jens Kockskämper
Hypertensive heart disease (HHD) can cause left ventricular (LV) hypertrophy and heart failure (HF). It is unclear, though, which factors may contribute to the transition from compensated LV hypertrophy to HF in HHD. We hypothesized that maladaptive atrial remodeling with impaired atrial myocyte function would occur in advanced HHD and may be associated with the emergence of HF. Experiments were performed on atrial myocytes and tissue from old (15-25months) normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with advanced HHD...
November 27, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29180047/iron-status-and-oxidative-stress-in-the-aged-rabbit-heart
#8
Domenico Lapenna, Giuliano Ciofani, Sante Donato Pierdomenico, Maria Adele Giamberardino, Ettore Porreca
Altered iron status may be relevant to the pathophysiology of aging. We have assessed redox-active catalytic low molecular weight iron (LMWI), non-heme iron (NHI), heme iron (HI), and total iron (TI) in the aerobically perfused hearts of aged rabbits (AR, about 4.5years old) and young adult control rabbits (YACR, 3-4months old); myocardial lipid and protein oxidation were also assessed as oxidative stress biomarkers. The levels of LMWI and NHI, as well as of lipid and protein oxidation, were higher, while HI content was lower, in the hearts of AR than in those of YACR; TI did not differ significantly between the two groups...
November 24, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29175505/characteristics-of-induced-pluripotent-stem-cells-from-clinically-divergent-female-monozygotic-twins-with-danon-disease
#9
Shohei Yoshida, Chiaki Nakanishi, Hirofumi Okada, Masayuki Mori, Junichiro Yokawa, Tsuyoshi Yoshimuta, Kunio Ohta, Tetsuo Konno, Noboru Fujino, Masa-Aki Kawashiri, Akihiro Yachie, Masakazu Yamagishi, Kenshi Hayashi
RATIONALE: Induced pluripotent stem cells (iPSCs) have been generated from patients with various forms of disease, including Danon disease (DD); however, few reports exist regarding disease-specific iPSCs derived from clinically divergent monozygotic twins. OBJECTIVE: We examined the characteristics of iPSCs and iPSC-derived cardiomyocytes (iPSC-CMs) generated from clinically divergent monozygotic female twins with DD. METHODS AND RESULTS: We generated iPSCs derived from T-cells isolated from clinically divergent, 18-year-old female twins with DD harboring a mutation in LAMP2 at the intron 6 splice site (IVS6+1_4delGTGA)...
November 23, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29174768/acetylation-of-tbx5-by-kat2b-and-kat2a-regulates-heart-and-limb-development
#10
Tushar K Ghosh, José J Aparicio-Sánchez, Sarah Buxton, Ami Ketley, Tasabeeh Mohamed, Catrin S Rutland, Siobhan Loughna, J David Brook
TBX5 plays a critical role in heart and forelimb development. Mutations in TBX5 cause Holt-Oram syndrome, an autosomal dominant condition that affects the formation of the heart and upper-limb. Several studies have provided significant insight into the role of TBX5 in cardiogenesis; however, how TBX5 activity is regulated by other factors is still unknown. Here we report that histone acetyltransferases KAT2A and KAT2B associate with TBX5 and acetylate it at Lys339. Acetylation potentiates its transcriptional activity and is required for nuclear retention...
November 22, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29174767/sorcin-ablation-plus-%C3%AE-adrenergic-stimulation-generate-an-arrhythmogenic-substrate-in-mouse-ventricular-myocytes
#11
Xi Chen, Craig Weber, Emily T Farrell, Francisco J Alvarado, Yan-Ting Zhao, Ana M Gómez, Héctor H Valdivia
Sorcin, a penta-EF hand Ca2+-binding protein expressed in cardiomyocytes, is known to interact with ryanodine receptors and other Ca2+ regulatory proteins. To investigate sorcin's influence on cardiac excitation-contraction coupling and its role in the development of cardiac malfunctions, we generated a sorcin knockout (KO) mouse model. Sorcin KO mice presented ventricular arrhythmia and sudden death when challenged by acute stress induced by isoproterenol plus caffeine. Chronic stress, which was induced by transverse aortic constriction, significantly decreased the survival rate of sorcin KO mice...
November 22, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29175286/microrna-34a-modulates-the-notch-signaling-pathway-in-mice-with-congenital-heart-disease-and-its-role-in-heart-development
#12
Kai-Hong Wu, Qian-Ru Xiao, Yu Yang, Jia-Li Xu, Feng Zhang, Chao-Ming Liu, Zhao-Ming Zhang, Ying-Qi Lu, Ning-Ping Huang
The objective of the study was to elucidate the mechanism by which microRNA-34a (miR-34a) influences heart development and participates in the pathogenesis of congenital heart disease (CHD) by targeting NOTCH-1 through the Notch signaling pathway. Forty D7 pregnant mice were recruited for the purposes of the study and served as the CHD (n=20, successfully established as CHD model) and normal (n=20) groups. The positive expression of the NOTCH-1 protein was evaluated by means of immunohistochemistry. Embryonic endocardial cells (ECCs) were assigned into the normal, blank, negative control (NC), miR-34a mimics, miR-34a inhibitors, miR-34a inhibitors+siRNA-NOTCH-1, siRNA-NOTCH-1, miR-34a mimics+NOTCH-1 OE and miR-34a mimics+crispr/cas9 (mutant NOTCH-1) groups...
November 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29169992/hax-1-regulates-serca2a-oxidation-and-degradation
#13
Philip A Bidwell, Guan-Sheng Liu, Narayani Nagarajan, Chi Keung Lam, Kobra Haghighi, George Gardner, Wen-Feng Cai, Wen Zhao, Luke Mugge, Elizabeth Vafiadaki, Despina Sanoudou, Jack Rubinstein, Djamel Lebeche, Roger Hajjar, Junichi Sadoshima, Evangelia G Kranias
Ischemia/reperfusion injury is associated with contractile dysfunction and increased cardiomyocyte death. Overexpression of the hematopoietic lineage substrate-1-associated protein X-1 (HAX-1) has been shown to protect from cellular injury but the function of endogenous HAX-1 remains obscure due to early lethality of the knockout mouse. Herein we generated a cardiac-specific and inducible HAX-1 deficient model, which uncovered an unexpected role of HAX-1 in regulation of sarco/endoplasmic reticulum Ca-ATPase (SERCA2a) in ischemia/reperfusion injury...
November 20, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29158034/different-notch-signaling-in-cells-from-calcified-bicuspid-and-tricuspid-aortic-valves
#14
A Kostina, A Shishkova, E Ignatieva, O Irtyuga, M Bogdanova, K Levchuk, A Golovkin, E Zhiduleva, V Uspenskiy, O Moiseeva, G Faggian, J Vaage, A Kostareva, A Rutkovskiy, A Malashicheva
AIMS: Calcific aortic valve disease is the most common heart valve disease in the Western world. Bicuspid and tricuspid aortic valve calcifications are traditionally considered together although the dynamics of the disease progression is different between the two groups of patients. Notch signaling is critical for bicuspid valve development and NOTCH1 mutations are associated with bicuspid valve and calcification. We hypothesized that Notch-dependent mechanisms of valve mineralization might be different in the two groups...
November 17, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29158033/resident-fibroblast-expansion-during-cardiac-growth-and-remodeling
#15
Malina J Ivey, Jill T Kuwabara, Jonathan T Pai, Richard E Moore, Zuyue Sun, Michelle D Tallquist
Cardiac fibrosis, denoted by the deposition of extracellular matrix, manifests with a variety of diseases such as hypertension, diabetes, and myocardial infarction. Underlying this pathological extracellular matrix secretion is an expansion of fibroblasts. The mouse is now a common experimental model system for the study of cardiovascular remodeling and elucidation of fibroblast responses to cardiac growth and stress is vital for understanding disease processes. Here, using diverse but fibroblast specific markers, we report murine fibroblast distribution and proliferation in early postnatal, adult, and injured hearts...
November 17, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29155072/a-protocol-to-study-ex-vivo-mouse-working-heart-at-human-like-heart-rate
#16
Han-Zhong Feng, Jian-Ping Jin
Genetically modified mice are widely used as experimental models to study human heart function and diseases. However, the fast rate of normal mouse heart at 400-600bpm limits its capacity of assessing kinetic parameters that are important for the physiology and pathophysiology of human heart that beats at a much slower rate (75-180bpm). To extend the value of mouse models, we established a protocol to study ex vivo mouse working hearts at a human-like heart rate. In the presence of 300μM lidocaine to lower pacemaker and conductive activities and prevent arrhythmia, a stable rate of 120-130bpm at 37°C is achieved for ex vivo mouse working hearts...
November 16, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29155025/understanding-the-role-of-mammalian-sterile-20-like-kinase-1-mst1-in-cardiovascular-disorders
#17
REVIEW
Yang Yang, Haichang Wang, Zhiqiang Ma, Wei Hu, Dongdong Sun
Hippo signaling is a conserved pathway and plays important role in controlling cell proliferation and differentiation. As critical components of the Hippo pathway in mammals, mammalian sterile 20-like kinase 1 (MST1) participate in cell apoptosis and cell proliferation. Yes-associated protein (YAP) acts as a downstream transcriptional co-activator of MST1. MST1 is present in heart tissue and helps determine the fate of cardiomyocytes by regulating the balance between autophagy and apoptosis. Recent studies showed MST1 signaling is an essential participant in many cardiovascular disorders, including aortic dissection, aortic aneurysm, atherosclerosis, myocardial ischemic injury, and cardiomyopathy...
November 15, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29154780/the-feedback-loop-of-emmprin-nf-%C3%AE%C2%BAb-worsens-atherosclerotic-plaque-via-suppressing-autophagy-in-macrophage
#18
Xing Liang, Xianhua Hou, Yang Yang, Hong Liu, Ruiwei Guo, Zhihua Yang, Lixia Yang
This study examined the significance of macrophage autophagy in extracellular matrix metalloproteinase inducer (EMMPRIN)-mediated atherosclerosis (AS). Apolipoprotein E-deficient (ApoE-/-) mice were fed a western diet to establish an AS model. EMMPRIN and p62/Sequestosome-1(SQSTM1) expression were evaluated in plaque macrophages from the AS mice using immunofluorescence. The EMMPRIN and p62/SQSTM1 protein expression levels in macrophages increased with the increasing vulnerability of the atherosclerotic plaques...
November 14, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29146153/the-stress-kinase-jnk-regulates-gap-junction-cx43-gene-expression-and-promotes-atrial-fibrillation-in-the-aged-heart
#19
Jiajie Yan, Justin K Thomson, Weiwei Zhao, Xiaomin Wu, Xianlong Gao, Dominic DeMarco, Wei Kong, Min Tong, Jun Sun, Mamdouh Bakhos, Vladimir G Fast, Qingrong Liang, Sumanth D Prabhu, Xun Ai
BACKGROUND: The stress kinase c-jun N-terminal kinase (JNK) is critical in the pathogenesis of cardiac diseases associated with an increased incidence of atrial fibrillation (AF), the most common arrhythmia in the elderly. We recently discovered that JNK activation is linked to the loss of gap junction connexin43 (Cx43) and enhanced atrial arrhythmogenicity. However, direct evidence for JNK-mediated impairment of intercellular coupling (cell-cell communication) in the intact aged atrium is lacking, as is evidence for whether and how JNK suppresses Cx43 in the aged human atrium...
November 13, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29141185/increased-cross-bridge-recruitment-contributes-to-transient-increase-in-force-generation-beyond-maximal-capacity-in-human-myocardium
#20
Nima Milani-Nejad, Jae-Hoon Chung, Benjamin D Canan, Vadim V Fedorov, Bryan A Whitson, Ahmet Kilic, Peter J Mohler, Paul M L Janssen
Cross-bridge attachment allows force generation to occur, and rate of tension redevelopment (ktr) is a commonly used index of cross-bridge cycling rate. Tension overshoots have been observed briefly after a slack-restretch ktr maneuver in various species of animal models and humans. In this study, we set out to determine the properties of these overshoots and their possible underlying mechanism. Utilizing human cardiac trabeculae, we have found that tension overshoots are temperature-dependent and that they do not occur at resting states...
November 12, 2017: Journal of Molecular and Cellular Cardiology
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