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Turnover of cardiomyocytes

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https://www.readbyqxmd.com/read/29875314/hsc70-is-a-chaperone-for-wild-type-and-mutant-cardiac-myosin-binding-protein-c
#1
Amelia A Glazier, Neha Hafeez, Dattatreya Mellacheruvu, Venkatesha Basrur, Alexey I Nesvizhskii, Lap Man Lee, Hao Shao, Vi Tang, Jaime M Yob, Jason E Gestwicki, Adam S Helms, Sharlene M Day
Cardiac myosin binding protein C (MYBPC3) is the most commonly mutated gene associated with hypertrophic cardiomyopathy (HCM). Haploinsufficiency of full-length MYBPC3 and disruption of proteostasis have both been proposed as central to HCM disease pathogenesis. Discriminating the relative contributions of these 2 mechanisms requires fundamental knowledge of how turnover of WT and mutant MYBPC3 proteins is regulated. We expressed several disease-causing mutations in MYBPC3 in primary neonatal rat ventricular cardiomyocytes...
June 7, 2018: JCI Insight
https://www.readbyqxmd.com/read/29862928/molecular-basis-of-functional-myogenic-specification-of-bona-fide-multipotent-adult-cardiac-stem-cells
#2
Eleonora Cianflone, Iolanda Aquila, Mariangela Scalise, Pina Marotta, Michele Torella, Bernardo Nadal-Ginard, Daniele Torella
Ischemic Heart Disease (IHD) remains the developed world's number one killer. The improved survival from Acute Myocardial Infarction (AMI) and the progressive aging of western population brought to an increased incidence of chronic Heart Failure (HF), which assumed epidemic proportions nowadays. Except for heart transplantation, all treatments for HF should be considered palliative because none of the current therapy can reverse myocardial degeneration responsible for HF syndrome. To stop the HF epidemic will ultimately require protocols to reduce the progressive cardiomyocyte (CM) loss and to foster their regeneration...
June 3, 2018: Cell Cycle
https://www.readbyqxmd.com/read/29747586/selective-modulation-of-local-linkages-between-active-transcription-and-oxidative-demethylation-activity-shapes-cardiomyocyte-specific-gene-body-epigenetic-status-in-mice
#3
Mayumi Oda, Shunichi Wakabayashi, N Ari Wijetunga, Shinsuke Yuasa, Hirokazu Enomoto, Ruri Kaneda, Sung Han Yoon, Nishant Mittal, Qiang Jing, Masako Suzuki, John M Greally, Keiichi Fukuda, Shinji Makino
BACKGROUND: Cell-type-specific genes exhibit heterogeneity in genomic contexts and may be subject to different epigenetic regulations through different gene transcriptional processes depending on the cell type involved. The gene-body regions (GBRs) of some cardiomyocyte (CM)-specific genes are long and highly hypomethylated in CMs. To explore the cell-type specificities of epigenetic patterns and functions, multiple epigenetic modifications of GBRs were compared among CMs, liver cells and embryonic stem cells (ESCs)...
May 10, 2018: BMC Genomics
https://www.readbyqxmd.com/read/29703225/cardiopulmonary-bypass-reduces-myocardial-oxidative-stress-inflammation-and-increases-c-kit-cd45-cell-population-in-newborns
#4
Johannes Petersen, Andrey Kazakov, Michael Böhm, Hans-Joachim Schäfers, Ulrich Laufs, Hashim Abdul-Khaliq
BACKGROUND: The aim of this study was to characterize the influence of cardiopulmonary bypass (CPB) on myocardial remodeling in newborns and children. METHODS: Biopsies from the right atrium were taken before and after CPB from 4 newborns (5-11 days old) and 7 children (8 months-16 years old). Immunostainings on 10 µm heart tissue frozen sections were performed to detect c-kit+ cells, leukocytes (CD45+ cells), Ki67+ cycling cells. The percentage of 8-hydroxy-guanosine (8-dOHG)+ cardiomyocytes and non-cardiomyocytes [(8-dOHG)+ -index] were determined to quantify oxidative stress...
April 27, 2018: Journal of Translational Medicine
https://www.readbyqxmd.com/read/29691397/non-invasive-detection-of-human-cardiomyocyte-death-using-methylation-patterns-of-circulating-dna
#5
Hai Zemmour, David Planer, Judith Magenheim, Joshua Moss, Daniel Neiman, Dan Gilon, Amit Korach, Benjamin Glaser, Ruth Shemer, Giora Landesberg, Yuval Dor
Detection of cardiomyocyte death is crucial for the diagnosis and treatment of heart disease. Here we use comparative methylome analysis to identify genomic loci that are unmethylated specifically in cardiomyocytes, and develop these as biomarkers to quantify cardiomyocyte DNA in circulating cell-free DNA (cfDNA) derived from dying cells. Plasma of healthy individuals contains essentially no cardiomyocyte cfDNA, consistent with minimal cardiac turnover. Patients with acute ST-elevation myocardial infarction show a robust cardiac cfDNA signal that correlates with levels of troponin and creatine phosphokinase (CPK), including the expected elevation-decay dynamics following coronary angioplasty...
April 24, 2018: Nature Communications
https://www.readbyqxmd.com/read/29577900/protective-effects-of-kenpaullone-on-cardiomyocytes-following-h-2-o-2-induced-oxidative-stress-are-attributed-to-inhibition-of-connexin-43-degradation-by-sgsm3
#6
Hyun-Chel Joo, Jung-Won Choi, Hanbyeol Moon, Chang Youn Lee, Kyung-Jong Yoo, Sang Woo Kim, Ki-Chul Hwang
A previous study showed that small G protein signaling modulator 3 (SGSM3) was highly correlated with Cx43 in heart functions and that high levels of SGSM3 may induce Cx43 turnover through lysosomal degradation in infarcted rat hearts. Here, we investigated the protective effects of kenpaullone on cardiomyocytes following H2 O2 -induced oxidative stress mediated by the interaction of SGSM3 with Cx43. We found that the gap junction protein Cx43 was significantly down-regulated in an H2 O2 concentration-dependent manner, whereas expression of SGSM3 was up-regulated upon H2 O2 exposure in H9c2 cells...
May 5, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29203715/the-role-of-heat-shock-proteins-and-co-chaperones-in-heart-failure
#7
REVIEW
Mark J Ranek, Marisa J Stachowski, Jonathan A Kirk, Monte S Willis
The ongoing contractile and metabolic demands of the heart require a tight control over protein quality control, including the maintenance of protein folding, turnover and synthesis. In heart disease, increases in mechanical and oxidative stresses, post-translational modifications (e.g., phosphorylation), for example, decrease protein stability to favour misfolding in myocardial infarction, heart failure or ageing. These misfolded proteins are toxic to cardiomyocytes, directly contributing to the common accumulation found in human heart failure...
January 19, 2018: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
https://www.readbyqxmd.com/read/29187824/the-implication-of-pgc-1%C3%AE-on-fatty-acid-transport-across-plasma-and-mitochondrial-membranes-in-the-insulin-sensitive-tissues
#8
REVIEW
Elżbieta Supruniuk, Agnieszka Mikłosz, Adrian Chabowski
PGC-1α coactivator plays a decisive role in the maintenance of lipid balance via engagement in numerous metabolic processes (i.e., Krebs cycle, β-oxidation, oxidative phosphorylation and electron transport chain). It constitutes a link between fatty acids import and their complete oxidation or conversion into bioactive fractions through the coordination of both the expression and subcellular relocation of the proteins involved in fatty acid transmembrane movement. Studies on cell lines and/or animal models highlighted the existence of an upregulation of the total and mitochondrial FAT/CD36, FABPpm and FATPs content in skeletal muscle in response to PGC-1α stimulation...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/29069231/myostatin-promotes-distinct-responses-on-protein-metabolism-of-skeletal-and-cardiac-muscle-fibers-of-rodents
#9
L H Manfredi, S Paula-Gomes, N M Zanon, I C Kettelhut
Myostatin is a novel negative regulator of skeletal muscle mass. Myostatin expression is also found in heart in a much less extent, but it can be upregulated in pathological conditions, such as heart failure. Myostatin may be involved in inhibiting protein synthesis and/or increasing protein degradation in skeletal and cardiac muscles. Herein, we used cell cultures and isolated muscles from rats to determine protein degradation and synthesis. Muscles incubated with myostatin exhibited an increase in proteolysis with an increase of Atrogin-1, MuRF1 and LC3 genes...
October 19, 2017: Brazilian Journal of Medical and Biological Research, Revista Brasileira de Pesquisas Médicas e Biológicas
https://www.readbyqxmd.com/read/28810672/cardiomyocyte-renewal-in-the-human-heart-insights-from-the-fall-out
#10
Eniko Lázár, Hesham A Sadek, Olaf Bergmann
The capacity of the mammalian heart to regenerate cardiomyocytes has been debated over the last decades. However, limitations in existing techniques to track and identify nascent cardiomyocytes have often led to inconsistent results. Radiocarbon (14C) birth dating, in combination with other quantitative strategies, allows to establish the number and age of human cardiomyocytes, making it possible to describe their age distribution and turnover dynamics. Accurate estimates of cardiomyocyte generation in the adult heart can provide the foundation for novel regenerative strategies that aim to stimulate cardiomyocyte renewal in various cardiac pathologies...
August 7, 2017: European Heart Journal
https://www.readbyqxmd.com/read/28716730/interaction-of-small-g-protein-signaling-modulator-3-with-connexin-43-contributes-to-myocardial-infarction-in-rat-hearts
#11
Chang Youn Lee, Jung-Won Choi, Sunhye Shin, Jiyun Lee, Hyang-Hee Seo, Soyeon Lim, Seahyoung Lee, Hyun-Chul Joo, Sang Woo Kim, Ki-Chul Hwang
Connexin 43 (Cx43), a ubiquitous connexin expressed in the heart and skin, is associated with a variety of hereditary conditions. Therefore, the characterization of Cx43-interacting proteins and their dynamics is important to understand not only the molecular mechanisms underlying pathological malfunction of gap junction-mediated intercellular communication but also to identify novel and unanticipated biological functions of Cx43. In the present study, we observed potential targets of Cx43 to determine new molecular functions in cardio-protection...
September 16, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28684531/cardiomyocyte-regeneration-a-consensus-statement
#12
REVIEW
Thomas Eschenhagen, Roberto Bolli, Thomas Braun, Loren J Field, Bernd K Fleischmann, Jonas Frisén, Mauro Giacca, Joshua M Hare, Steven Houser, Richard T Lee, Eduardo Marbán, James F Martin, Jeffery D Molkentin, Charles E Murry, Paul R Riley, Pilar Ruiz-Lozano, Hesham A Sadek, Mark A Sussman, Joseph A Hill
No abstract text is available yet for this article.
August 15, 2017: Circulation
https://www.readbyqxmd.com/read/28658286/mybpc3-mutations-are-associated-with-a-reduced-super-relaxed-state-in-patients-with-hypertrophic-cardiomyopathy
#13
James W McNamara, Amy Li, Sean Lal, J Martijn Bos, Samantha P Harris, Jolanda van der Velden, Michael J Ackerman, Roger Cooke, Cristobal G Dos Remedios
The "super-relaxed state" (SRX) of myosin represents a 'reserve' of motors in the heart. Myosin heads in the SRX are bound to the thick filament and have a very low ATPase rate. Changes in the SRX are likely to modulate cardiac contractility. We previously demonstrated that the SRX is significantly reduced in mouse cardiomyocytes lacking cardiac myosin binding protein-C (cMyBP-C). Here, we report the effect of mutations in the cMyBP-C gene (MYBPC3) using samples from human patients with hypertrophic cardiomyopathy (HCM)...
2017: PloS One
https://www.readbyqxmd.com/read/28550172/myocardial-overexpression-of-timp3-after-myocardial-infarction-exerts-beneficial-effects-by-promoting-angiogenesis-and-suppressing-early-proteolysis
#14
Abhijit Takawale, Pu Zhang, Abul Azad, Wang Wang, Xiuhua Wang, Allan G Murray, Zamaneh Kassiri
Myocardial infarction (MI) results in loss of cardiomyocytes, adverse extracellular matrix (ECM) and structural remodeling, and left ventricular (LV) dilation and dysfunction. Tissue inhibitors of metalloproteinase (TIMPs) inhibit matrix metalloproteinases (MMPs), the main regulators of ECM turnover. TIMPs also have MMP-independent functions. TIMP3 levels are reduced in the heart within 24 h of MI in mice. We investigated if overexpression of TIMP3 post-MI limits adverse remodeling and LV dilation and dysfunction...
August 1, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28522833/parkin-regulation-of-chop-modulates-susceptibility-to-cardiac-endoplasmic-reticulum-stress
#15
Kim Han, Shahin Hassanzadeh, Komudi Singh, Sara Menazza, Tiffany T Nguyen, Mark V Stevens, An Nguyen, Hong San, Stasia A Anderson, Yongshun Lin, Jizhong Zou, Elizabeth Murphy, Michael N Sack
The regulatory control of cardiac endoplasmic reticulum (ER) stress is incompletely characterized. As ER stress signaling upregulates the E3-ubiquitin ligase Parkin, we investigated the role of Parkin in cardiac ER stress. Parkin knockout mice exposed to aortic constriction-induced cardiac pressure-overload or in response to systemic tunicamycin (TM) developed adverse ventricular remodeling with excessive levels of the ER regulatory C/EBP homologous protein CHOP. CHOP was identified as a Parkin substrate and its turnover was Parkin-dose and proteasome-dependent...
May 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28413577/circadian-control-of-cardiac-metabolism-physiologic-roles-and-pathologic-implications
#16
REVIEW
Martin E Young
Over the course of the day, the heart is challenged with dramatic fluctuations in energetic demand and nutrient availability. It is therefore not surprising that rhythms in cardiac metabolism have been reported at multiple levels, including the utilization of glucose, fatty acids, and amino acids. Evidence has emerged suggesting that the cardiomyocyte circadian clock is in large part responsible for governing cardiac metabolic rhythms. In doing so, the cardiomyocyte clock temporally partitions ATP generation for increased contractile function during the active period, promotes nutrient storage at the end of the active period, and facilitates protein turnover (synthesis and degradation) during the beginning of the sleep phase...
January 2017: Methodist DeBakey Cardiovascular Journal
https://www.readbyqxmd.com/read/28376509/activation-of-g%C3%AE-q-in-cardiomyocytes-increases-vps34-activity-and-stimulates-autophagy
#17
Shengnan Liu, Ya-Ping Jiang, Lisa M Ballou, Wei-Xing Zong, Richard Z Lin
Receptors that activate the heterotrimeric G protein Gαq are thought to play a role in the development of heart failure. Dysregulation of autophagy occurs in some pathological cardiac conditions including heart failure, but whether Gαq is involved in this process is unknown. We used a cardiomyocyte-specific transgenic mouse model of inducible Gαq activation (termed GαqQ209L) to address this question. After 7 days of Gαq activation, GαqQ209L hearts contained more autophagic vacuoles than wild type hearts...
April 2017: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28321411/different-densities-of-na-ca-exchange-current-in-t-tubular-and-surface-membranes-and-their-impact-on-cellular-activity-in-a-model-of-rat-ventricular-cardiomyocyte
#18
M Pásek, J Šimurda, G Christé
The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values of INaCa and membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the INaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28287537/visualization-of-cell-cycle-variations-and-determination-of-nucleation-in-postnatal-cardiomyocytes
#19
Alexandra Raulf, Nadine Voeltz, Daniel Korzus, Bernd K Fleischmann, Michael Hesse
Cardiomyocytes are prone to variations of the cell cycle, such as endoreduplication (continuing rounds of DNA synthesis without karyokinesis and cytokinesis) and acytokinetic mitosis (karyokinesis but no cytokinesis). Such atypical cell cycle variations result in polyploid and multinucleated cells rather than in cell division. Therefore, to determine cardiac turnover and regeneration, it is of crucial importance to correctly identify cardiomyocyte nuclei, the number of nuclei per cell, and their cell cycle status...
February 24, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28145902/redirecting-cardiac-growth-mechanisms-for-therapeutic-regeneration
#20
REVIEW
Ravi Karra, Kenneth D Poss
Heart failure is a major source of morbidity and mortality. Replacing lost myocardium with new tissue is a major goal of regenerative medicine. Unlike adult mammals, zebrafish and neonatal mice are capable of heart regeneration following cardiac injury. In both contexts, the regenerative program echoes molecular and cellular events that occur during cardiac development and morphogenesis, notably muscle creation through division of cardiomyocytes. Based on studies over the past decade, it is now accepted that the adult mammalian heart undergoes a low grade of cardiomyocyte turnover...
February 1, 2017: Journal of Clinical Investigation
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