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https://www.readbyqxmd.com/read/29431258/human-cardiomyocyte-calcium-handling-and-transverse-tubules-in-mid-stage-of-post-myocardial-infarction-heart-failure
#1
Morten Andre Høydal, Idar Kirkeby-Garstad, Asbjørn Karevold, Rune Wiseth, Rune Haaverstad, Alexander Wahba, Tomas L Stølen, Riccardo Contu, Gianluigi Condorelli, Øyvind Ellingsen, Godfrey L Smith, Ole J Kemi, Ulrik Wisløff
AIMS: Cellular processes in the heart rely mainly on studies from experimental animal models or explanted hearts from patients with terminal end-stage heart failure (HF). To address this limitation, we provide data on excitation contraction coupling, cardiomyocyte contraction and relaxation, and Ca2+ handling in post-myocardial-infarction (MI) patients at mid-stage of HF. METHODS AND RESULTS: Nine MI patients and eight control patients without MI (non-MI) were included...
February 12, 2018: ESC Heart Failure
https://www.readbyqxmd.com/read/29407107/protection-against-reperfusion-injury-by-3-4-dihydroxyflavonol-in-rat-isolated-hearts-involves-inhibition-of-phospholamban-and-jnk2
#2
Kai Yee Chin, Lokugan S Silva, Ian A Darby, Dominic C H Ng, Owen L Woodman
BACKGROUND: Flavonols, including 3',4'-dihydroxyflavonol (DiOHF), reduce myocardial ischemia and reperfusion (I/R) injury but their mechanism remains uncertain. To better understand the mechanism of the cardioprotective actions of flavonols we investigated the effect of DiOHF on cardiac function and the activation of protective and injurious signalling kinases after I/R in rat isolated hearts. METHODS: We assessed the effect of global ischemia (20min) and reperfusion (5-30min) on cardiac function and injury in rat isolated, perfused hearts in the absence or presence of DiOHF (10μM) during reperfusion...
March 1, 2018: International Journal of Cardiology
https://www.readbyqxmd.com/read/29403384/phenotyping-of-mice-with-heart-specific-overexpression-of-a2a-adenosine-receptors-evidence-for-cardioprotective-effects-of-a2a-adenosine-receptors
#3
Peter Boknik, Katharina Drzewiecki, John Eskandar, Ulrich Gergs, Stephanie Grote-Wessels, Larissa Fabritz, Paulus Kirchhof, Frank U Müller, Frank Stümpel, Wilhelm Schmitz, Norbert Zimmermann, Uwe Kirchhefer, Joachim Neumann
Background: Adenosine can be produced in the heart and acts on cardiac adenosine receptors. One of these receptors is the A2A-adenosine receptor (A2A-AR). Methods and Results: To better understand its role in cardiac function, we generated and characterized mice (A2A-TG) which overexpress the human A2A-AR in cardiomyocytes. In isolated atrial preparations from A2A-TG but not from WT, CGS 21680, an A2A-AR agonist, exerted positive inotropic and chronotropic effects. In ventricular preparations from A2A-TG but not WT, CGS 21680 increased the cAMP content and the phosphorylation state of phospholamban and of the inhibitory subunit of troponin in A2A-TG but not WT...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29371236/crabp1-protects-the-heart-from-isoproterenol-induced-acute-and-chronic-remodeling
#4
Sung Wook Park, Shawna D Persaud, Stanislas Ogokeh, Tatyana A Meyers, DeWayne Townsend, Li Na Wei
Excessive and/or persistent activation of calcium-calmodulin protein kinase II (CaMKII) is detrimental in acute and chronic cardiac injury. However, intrinsic regulators of CaMKII activity are poorly understood. We find that cellular retinoic acid binding protein 1 (CRABP1) directly interacts with CaMKII, and uncover a functional role for CRABP1 in regulating CaMKII activation. We generated Crabp1 null mice (CKO) in C57BL/6J background for pathophysiological studies. CKO mice develop hypertrophy as adults, exhibiting significant left ventricular dilation with reduced ejection fraction at the baseline cardiac function...
January 25, 2018: Journal of Endocrinology
https://www.readbyqxmd.com/read/29350681/aav-9-mediated-phosphatase-1-inhibitor-1-overexpression-improves-cardiac-contractility-in-unchallenged-mice-but-is-deleterious-in-pressure-overload
#5
D M Schwab, L Tilemann, R Bauer, M Heckmann, A Jungmann, M Wagner, J Burgis, C Vettel, H A Katus, A El-Armouche, O J Müller
The downregulation of β-adrenergic receptors (β-AR) and decreased cAMP-dependent protein kinase activity in failing hearts results in decreased phosphorylation and inactivation of phosphatase-inhibitor-1 (I-1), a distal amplifier element of β-adrenergic signaling, leading to increased protein phosphatase 1 activity and dephosphorylation of key phosphoproteins, including phospholamban. Downregulated and hypophosphorylated I-1 likely contributes to β-AR desensitization; therefore its modulation is a promising approach in heart failure treatment...
January 2018: Gene Therapy
https://www.readbyqxmd.com/read/29325795/insertional-mutagenesis-confounds-the-mechanism-of-the-morbid-phenotype-of-a-plnr9c-transgenic-mouse-line
#6
Alexander Kraev
BACKGROUND: A mouse line with heterozygous transgenic expression of phospholamban carrying a substitution of cysteine for arginine 9 (TgPLNR9C) under the control of α-myosin heavy chain (αMHC) promoter features dilated cardiomyopathy, heart failure and premature death. METHODS AND RESULTS: Determination of transgene chromosomal localization by conventional methods shows that in this line the transgenic array of 13 PLNR9C expression cassettes, arranged in a head-to-tail tandem orientation, has integrated into the bi-directional promoter of the αMHC (Myh6) gene and the gene for the regulatory non-coding RNA Myheart (Mhrt), both of which are known to be involved in cardiac development and pathology...
January 8, 2018: Journal of Cardiac Failure
https://www.readbyqxmd.com/read/29273673/reduced-serca-activity-underlies-dysregulation-of-ca2-homeostasis-under-atmospheric-o2-levels
#7
Thomas P Keeley, Richard C M Siow, Ron Jacob, Giovanni E Mann
Unregulated increases in cellular Ca2+ homeostasis are a hallmark of pathophysiological conditions and a key trigger of cell death. Endothelial cells cultured under physiologic O2 conditions (5% O2) exhibit a reduced cytosolic Ca2+ response to stimulation. The mechanism for reduced plateau [Ca2+]i upon stimulation was due to increased sarco/endoplasmic reticulum Ca2+ ATPase (SERCA)-mediated reuptake rather than changes in Ca2+ influx capacity. Agonist-stimulated phosphorylation of the SERCA regulatory protein phospholamban was increased in cells cultured under 5% O2 Elevation of cytosolic and mitochondrial [Ca2+] and cell death after prolonged ionomycin treatment, as a model of Ca2+ overload, were lower when cells were cultured long-term under 5% compared with 18% O2 This protection was abolished by cotreatment with the SERCA inhibitor cyclopiazonic acid...
December 22, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29191788/progressive-impairment-of-atrial-myocyte-function-during-left-ventricular-hypertrophy-and-heart-failure
#8
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/29179218/puerarin-enhances-ca2-reuptake-and-ca2-content-of-sarcoplasmic-reticulum-in-murine-embryonic-stem-cell-derived-cardiomyocytes-via-upregulation-of-serca2a
#9
Lu Wang, Yurong Cui, Qinghua Liu, Yuanlong Song, Qinghua Hu, Ming Tang, Jürgen Hescheler, Jiaoya Xi
BACKGROUND/AIMS: The embryonic stem cell-derived cardiomyocytes (ES-CMs) serve as potential sources for cardiac regenerative therapy. However, the immature sarcoplasmic reticulum (SR) function of ES-CMs prevents its application. In this report, we examined the effect of puerarin, an isoflavone compound, on SR function of murine ES-CMs. METHODS: Murine ES-CMs were harvested by embryoid body-based differentiation method. Confocal calcium imaging and whole-cell patch clamps were performed to assess the function of SR...
November 28, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29173803/1h-detected-mas-solid-state-nmr-experiments-enable-the-simultaneous-mapping-of-rigid-and-dynamic-domains-of-membrane-proteins
#10
T Gopinath, Sarah E D Nelson, Gianluigi Veglia
Magic angle spinning (MAS) solid-state NMR (ssNMR) spectroscopy is emerging as a unique method for the atomic resolution structure determination of native membrane proteins in lipid bilayers. Although 13C-detected ssNMR experiments continue to play a major role, recent technological developments have made it possible to carry out 1H-detected experiments, boosting both sensitivity and resolution. Here, we describe a new set of 1H-detected hybrid pulse sequences that combine through-bond and through-space correlation elements into single experiments, enabling the simultaneous detection of rigid and dynamic domains of membrane proteins...
December 2017: Journal of Magnetic Resonance
https://www.readbyqxmd.com/read/29150445/the-antiapoptotic-protein-hax-1-mediates-half-of-phospholamban-s-inhibitory-activity-on-calcium-cycling-and-contractility-in-the-heart
#11
Philip A Bidwell, Kobra Haghighi, Evangelia G Kranias
The antiapoptotic protein HAX-1 (HS-associated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts with the small membrane protein phospholamban (PLN), inhibiting the cardiac sarco/endoplasmic reticulum calcium ATPase 2a (SERCA2a) in the regulation of overall calcium handling and heart muscle contractility. However, because global HAX-1 deletion causes early lethality, how much endogenous HAX-1 contributes to PLN's inhibitory activity on calcium cycling is unknown. We therefore generated a cardiac-specific and inducible knock-out mouse model...
January 5, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29140729/gene-expression-and-gene-associations-during-the-development-of-heart-failure-with-preserved-ejection-fraction-in-the-dahl-salt-sensitive-model-of-hypertension
#12
Jeffrey Yim, Hyokeun Cho, Simon W Rabkin
Gene expression and associations were examined in a model of heart failure with preserved ejection fraction (HFpEF), a condition with minimal effective treatment. Genes with at least two studies showing significant changes in Dahl rat with heart failure were examined by meta-analysis. Significantly increased in expression were iNOS, p47phox, ADM, ANP, OPN, ACE, MCP-1, GP91PHOX, ICAM-1, TGF-β1, CTGF, ET-1, p22phox, ETB, BNP, ETA, MMP13, Col1a1, MMP2, TIMP1, Col3a1, Il-1β, β-MHC, ECE1, MMP14, AGT, and MMP9...
November 15, 2017: Clinical and Experimental Hypertension: CHE
https://www.readbyqxmd.com/read/29119312/when-signalling-goes-wrong-pathogenic-variants-in-structural-and-signalling-proteins-causing-cardiomyopathies
#13
Mehroz Ehsan, He Jiang, Kate L Thomson, Katja Gehmlich
Cardiomyopathies are a diverse group of cardiac disorders with distinct phenotypes, depending on the proteins and pathways affected. A substantial proportion of cardiomyopathies are inherited and those will be the focus of this review article. With the wide application of high-throughput sequencing in the practice of clinical genetics, the roles of novel genes in cardiomyopathies are recognised. Here, we focus on a subgroup of cardiomyopathy genes [TTN, FHL1, CSRP3, FLNC and PLN, coding for Titin, Four and a Half LIM domain 1, Muscle LIM Protein, Filamin C and Phospholamban, respectively], which, despite their diverse biological functions, all have important signalling functions in the heart, suggesting that disturbances in signalling networks can contribute to cardiomyopathies...
November 8, 2017: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/29081402/conformational-memory-in-the-association-of-the-transmembrane-protein-phospholamban-with-the-sarcoplasmic-reticulum-calcium-pump-serca
#14
Serena Smeazzetto, Gareth P Armanious, Marai Rosa Moncelli, Jessi J Bak, M Joanne Lemieux, Howard S Young, Francesco Tadini-Buoninsegni
The sarcoplasmic reticulum Ca2+-ATPase SERCA promotes muscle relaxation by pumping calcium ions from the cytoplasm into the sarcoplasmic reticulum. SERCA activity is regulated by a variety of small transmembrane peptides, most notably by phospholamban in cardiac muscle and sarcolipin in skeletal muscle. However, how phospholamban and sarcolipin regulate SERCA is not fully understood. In the present study, we evaluated the effects of phospholamban and sarcolipin on calcium translocation and ATP hydrolysis by SERCA under conditions that mimic environments in sarcoplasmic reticulum membranes...
October 29, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29078377/growth-hormone-releasing-hormone-attenuates-cardiac-hypertrophy-and-improves-heart-function-in-pressure-overload-induced-heart-failure
#15
Iacopo Gesmundo, Michele Miragoli, Pierluigi Carullo, Letizia Trovato, Veronica Larcher, Elisa Di Pasquale, Mara Brancaccio, Marta Mazzola, Tania Villanova, Matteo Sorge, Marina Taliano, Maria Pia Gallo, Giuseppe Alloatti, Claudia Penna, Joshua M Hare, Ezio Ghigo, Andrew V Schally, Gianluigi Condorelli, Riccarda Granata
It has been shown that growth hormone-releasing hormone (GHRH) reduces cardiomyocyte (CM) apoptosis, prevents ischemia/reperfusion injury, and improves cardiac function in ischemic rat hearts. However, it is still not known whether GHRH would be beneficial for life-threatening pathological conditions, like cardiac hypertrophy and heart failure (HF). Thus, we tested the myocardial therapeutic potential of GHRH stimulation in vitro and in vivo, using GHRH or its agonistic analog MR-409. We show that in vitro, GHRH(1-44)NH 2 attenuates phenylephrine-induced hypertrophy in H9c2 cardiac cells, adult rat ventricular myocytes, and human induced pluripotent stem cell-derived CMs, decreasing expression of hypertrophic genes and regulating hypertrophic pathways...
November 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29068413/phospholamban-is-downregulated-by-pvhl-mediated-degradation-through-oxidative-stress-in-failing-heart
#16
Shunichi Yokoe, Michio Asahi
The E3 ubiquitin ligase, von Hippel-Lindau (VHL), regulates protein expression by polyubiquitination. Although the protein VHL (pVHL) was reported to be involved in the heart function, the underlying mechanism is unclear. Here, we show that pVHL was upregulated in hearts from two types of genetically dilated cardiomyopathy (DCM) mice models. In comparison with the wild-type mouse, both DCM mice models showed a significant reduction in the expression of phospholamban (PLN), a potent inhibitor of sarco(endo)plasmic reticulum Ca(2+)-ATPase, and enhanced interaction between pVHL and PLN...
October 25, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29057374/a-sarcoplasmic-reticulum-localized-protein-phosphatase-regulates-phospholamban-phosphorylation-and-promotes-ischemia-reperfusion-injury-in-the-heart
#17
Toru Akaike, Na Du, Gang Lu, Susumu Minamisawa, Yibin Wang, Hongmei Ruan
Phospholamban (PLN) is a key regulator of sarcolemma calcium uptake in cardiomyocyte, its inhibitory activity to SERCA is regulated by phosphorylation. PLN hypophosphorylation is a common molecular feature in failing heart. The current study provided evidence at molecular, cellular and whole heart levels to implicate a sarcolemma membrane targeted protein phosphatase, PP2Ce, as a specific and potent PLN phosphatase. PP2Ce expression was elevated in failing human heart and induced acutely at protein level by β -adrenergic stimulation or oxidative stress in cardiomyocytes...
March 2017: JACC. Basic to Translational Science
https://www.readbyqxmd.com/read/29045568/loss-of-protein-kinase-novel-1-pkn1-is-associated-with-mild-systolic-and-diastolic-contractile-dysfunction-increased-phospholamban-thr17-phosphorylation-and-exacerbated-ischaemia-reperfusion-injury
#18
Asvi A Francois, Kofo Obasanjo-Blackshire, James E Clark, Andrii Boguslavskyi, Mark R Holt, Peter Parker, Michael S Marber, Richard J Heads
Aims: PKN1 is a stress-responsive protein kinase acting downstream of small GTP-binding proteins of the Rho/Rac family. The aim was to determine its role in endogenous cardioprotection. Methods and Results: Hearts from PKN1 knockout (KO) or wild type (WT) littermate control mice were perfused in Langendorff mode and subjected to global ischemia and reperfusion (I/R). Myocardial infarct size was doubled in PKN1 KO hearts compared to WT hearts. PKN1 was basally phosphorylated on the activation loop Thr778 PDK1 target site which was unchanged during I/R...
October 16, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/29037982/early-effects-of-epac-depend-on-the-fine-tuning-of-the-sarcoplasmic-reticulum-ca-2-handling-in-cardiomyocytes
#19
N Lezcano, J I E Mariángelo, L Vittone, X H T Wehrens, M Said, C Mundiña-Weilenmann
In cardiac muscle, signaling through cAMP governs many fundamental cellular functions, including contractility, relaxation and automatism. cAMP cascade leads to the activation of the classic protein kinase A but also to the stimulation of the recently discovered exchange protein directly activated by cAMP (Epac). The role of Epac in the regulation of intracellular Ca(2+) homeostasis and contractility in cardiac myocytes is still matter of debate. In this study we showed that the selective Epac activator, 8-(4-chloro-phenylthio)-2'-O-methyladenosine-3', 5'-cyclic monophosphate (8-CPT), produced a positive inotropic effect when adult rat cardiac myocytes were stabilized at low [Ca(2+)]o (0...
October 14, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29030345/runx1-deficiency-protects-against-adverse-cardiac-remodeling-after-myocardial-infarction
#20
Charlotte S McCarroll, Weihong He, Kirsty Foote, Ashley Bradley, Karen Mcglynn, Francesca Vidler, Colin Nixon, Katrin Nather, Caroline Fattah, Alexandra Riddell, Peter Bowman, Elspeth B Elliott, Margaret Bell, Catherine Hawksby, Scott M MacKenzie, Liam J Morrison, Anne Terry, Karen Blyth, Godfrey L Smith, Martin W McBride, Thomas Kubin, Thomas Braun, Stuart A Nicklin, Ewan R Cameron, Christopher M Loughrey
BACKGROUND: Myocardial infarction (MI) is a leading cause of heart failure and death worldwide. Preservation of contractile function and protection against adverse changes in ventricular architecture (cardiac remodeling) are key factors to limiting progression of this condition to heart failure. Consequently, new therapeutic targets are urgently required to achieve this aim. Expression of the Runx1 transcription factor is increased in adult cardiomyocytes after MI; however, the functional role of Runx1 in the heart is unknown...
January 2, 2018: Circulation
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