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https://www.readbyqxmd.com/read/28228157/genetics-and-genomics-of-dilated-cardiomyopathy-and-systolic-heart-failure
#1
REVIEW
Upasana Tayal, Sanjay Prasad, Stuart A Cook
Heart failure is a major health burden, affecting 40 million people globally. One of the main causes of systolic heart failure is dilated cardiomyopathy (DCM), the leading global indication for heart transplantation. Our understanding of the genetic basis of both DCM and systolic heart failure has improved in recent years with the application of next-generation sequencing and genome-wide association studies (GWAS). This has enabled rapid sequencing at scale, leading to the discovery of many novel rare variants in DCM and of common variants in both systolic heart failure and DCM...
February 22, 2017: Genome Medicine
https://www.readbyqxmd.com/read/28214268/219th-enmc-international-workshop-titinopathies-international-database-of-titin-mutations-and-phenotypes-heemskerk-the-netherlands-29-april-1-may-2016
#2
Peter Hackman, Bjarne Udd, Carsten G Bönnemann, Ana Ferreiro
No abstract text is available yet for this article.
January 16, 2017: Neuromuscular Disorders: NMD
https://www.readbyqxmd.com/read/28213770/myosin-heavy-chain-and-cardiac-troponin-t-damage-is-associated-with-impaired-myofibrillar-atpase-activity-contributing-to-sarcomeric-dysfunction-in-ca-2-paradox-rat-hearts
#3
Árpád Kovács, Judit Kalász, Enikő T Pásztor, Attila Tóth, Zoltán Papp, Naranjan S Dhalla, Judit Barta
This study aimed to explore the potential contribution of myofibrils to contractile dysfunction in Ca(2+)-paradox hearts. Isolated rat hearts were perfused with Krebs-Henseleit solution (Control), followed by Ca(2+)-depletion, and then Ca(2+)-repletion after Ca(2+)-depletion (Ca(2+)-paradox) by Langendorff method. During heart perfusion left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of pressure development (+ dP/dt), and pressure decay (-dP/dt) were registered. Control LVDP (127...
February 17, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28173117/exploiting-the-crispr-cas9-system-to-study-alternative-splicing-in-vivo-application-to-titin
#4
Karine Charton, Laurence Suel, Sara F Henriques, Jean-Paul Moussu, Matteo Bovolenta, Miguel Taillepierre, Céline Becker, Karelia Lipson, Isabelle Richard
No abstract text is available yet for this article.
October 15, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/28151760/titin-truncating-mutations-in-dilated-cardiomyopathy-the-long-and-short-of-it
#5
Diane Fatkin, Inken G Huttner
PURPOSE OF REVIEW: Truncating variants in the TTN gene (TTNtv) are frequently identified in patients with dilated cardiomyopathy (DCM) but are also present in apparently healthy people in the general population. Consequently, there is considerable uncertainty about what it means for any single individual if a TTNtv is found. The aim of this review is to summarize current evidence implicating TTNtv in DCM pathogenesis and to provide some interpretative guidelines for clinical management...
February 1, 2017: Current Opinion in Cardiology
https://www.readbyqxmd.com/read/28101866/titin-and-nebulin-in-thick-and-thin-filament-length-regulation
#6
Larissa Tskhovrebova, John Trinick
In this review we discuss the history and the current state of ideas related to the mechanism of size regulation of the thick (myosin) and thin (actin) filaments in vertebrate striated muscles. Various hypotheses have been considered during of more than half century of research, recently mostly involving titin and nebulin acting as templates or 'molecular rulers', terminating exact assembly. These two giant, single-polypeptide, filamentous proteins are bound in situ along the thick and thin filaments, respectively, with an almost perfect match in the respective lengths and structural periodicities...
2017: Sub-cellular Biochemistry
https://www.readbyqxmd.com/read/28097712/force-generation-by-titin-folding
#7
Zsolt Mártonfalvi, Pasquale Bianco, Katalin Naftz, György G Ferenczy, Miklós Kellermayer
Titin is a giant protein that provides elasticity to muscle. As the sarcomere is stretched, titin extends hierarchically according to the mechanics of its segments. Whether titin's globular domains unfold during this process and how such unfolded domains might contribute to muscle contractility are strongly debated. To explore the force-dependent folding mechanisms, here we manipulated skeletal-muscle titin molecules with high-resolution optical tweezers. In force-clamp mode, after quenching the force (<10 pN), extension fluctuated without resolvable discrete events...
January 18, 2017: Protein Science: a Publication of the Protein Society
https://www.readbyqxmd.com/read/28096424/%C3%AE-actinin-titin-interaction-a-dynamic-and-mechanically-stable-cluster-of-bonds-in-the-muscle-z-disk
#8
Marco Grison, Ulrich Merkel, Julius Kostan, Kristina Djinović-Carugo, Matthias Rief
Stable anchoring of titin within the muscle Z-disk is essential for preserving muscle integrity during passive stretching. One of the main candidates for anchoring titin in the Z-disk is the actin cross-linker α-actinin. The calmodulin-like domain of α-actinin binds to the Z-repeats of titin. However, the mechanical and kinetic properties of this important interaction are still unknown. Here, we use a dual-beam optical tweezers assay to study the mechanics of this interaction at the single-molecule level...
January 31, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28092128/biomimetic-supramolecular-polymer-networks-exhibiting-both-toughness-and-self-recovery
#9
Ji Liu, Cindy Soo Yun Tan, Ziyi Yu, Yang Lan, Chris Abell, Oren A Scherman
Biomimetic supramolecular dual networks: By mimicking the structure/function model of titin, integration of dynamic cucurbit[8]uril mediated host-guest interactions with a trace amount of covalent cross-linking leads to hierarchical dual networks with intriguing toughness, strength, elasticity, and energy dissipation properties. Dynamic host-guest interactions can be dissociated as sacrificial bonds and their facile reformation results in self-recovery of the dual network structure as well as its mechanical properties...
January 16, 2017: Advanced Materials
https://www.readbyqxmd.com/read/28074486/introduction-of-steered-molecular-dynamics-into-unres-coarse-grained-simulations-package
#10
Adam K Sieradzan, Rafał Jakubowski
In this article, an implementation of steered molecular dynamics (SMD) in coarse-grain UNited RESidue (UNRES) simulations package is presented. Two variants of SMD have been implemented: with a constant force and a constant velocity. The huge advantage of SMD implementation in the UNRES force field is that it allows to pull with the speed significantly lower than the accessible pulling speed in simulations with all-atom representation of a system, with respect to a reasonable computational time. Therefore, obtaining pulling speed closer to those which appear in the atomic force spectroscopy is possible...
January 11, 2017: Journal of Computational Chemistry
https://www.readbyqxmd.com/read/28065693/inhibition-of-mir-208b-improves-cardiac-function-in-titin-based-dilated-cardiomyopathy
#11
Qifeng Zhou, Sonja Schötterl, Daniel Backes, Eva Brunner, Julia Kelley Hahn, Elena Ionesi, Parwez Aidery, Carsten Sticht, Siegfried Labeit, Reinhard Kandolf, Meinrad Gawaz, Michael Gramlich
BACKGROUND: Dilated cardiomyopathy (DCM) is the result of maladaptive cardiac remodeling, which involves microRNA regulation. In turn, microRNAs can contribute to the remodeling process by post-transcriptional modulation of gene expression networks. The exact role of microRNAs in the pathogenesis of DCM is largely unknown. Here, we used an inducible DCM mouse model that carries a human truncation mutation in the sarcomeric protein titin to dissect microRNA pathways in DCM development...
March 1, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28059474/csa-promotes-xist-expression-to-regulate-human-trophoblast-cells-proliferation-and-invasion-through-mir-144-titin-axis
#12
Nanhui Yu, Ying Liang, Hong Zhu, Hongying Mo, Haiping Pei
In our previous study, we revealed that Cyclosporin A (CsA) could inhibit miR-144 expression to regulate proliferation and invasion of human trophoblast (HT) cells through miR-144 targeting titin. This partially demonstrated the mechanism by which CsA promotes titin expression to increase the vitality of HT cells. However, the mechanism by which CsA inhibits miR-144 expression remains to be investigated. Recently, the interaction between lncRNA and miRNA has been frequently reported to play major role in several biological processes...
January 6, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28045975/titin-truncating-variants-in-dilated-cardiomyopathy-prevalence-and-genotype-phenotype-correlations
#13
Maria Franaszczyk, Przemyslaw Chmielewski, Grazyna Truszkowska, Piotr Stawinski, Ewa Michalak, Malgorzata Rydzanicz, Malgorzata Sobieszczanska-Malek, Agnieszka Pollak, Justyna Szczygieł, Joanna Kosinska, Adam Parulski, Tomasz Stoklosa, Agnieszka Tarnowska, Marcin M Machnicki, Bogna Foss-Nieradko, Malgorzata Szperl, Agnieszka Sioma, Mariusz Kusmierczyk, Jacek Grzybowski, Tomasz Zielinski, Rafal Ploski, Zofia T Bilinska
TTN gene truncating variants are common in dilated cardiomyopathy (DCM), although data on their clinical significance is still limited. We sought to examine the frequency of truncating variants in TTN in patients with DCM, including familial DCM (FDCM), and to look for genotype-phenotype correlations. Clinical cardiovascular data, family histories and blood samples were collected from 72 DCM probands, mean age of 34 years, 45.8% FDCM. DNA samples were examined by next generation sequencing (NGS) with a focus on the TTN gene...
2017: PloS One
https://www.readbyqxmd.com/read/28028799/residual-force-enhancement-is-regulated-by-titin-in-skeletal-and-cardiac-myofibrils
#14
Nabil Shalabi, Anabelle Cornachione, Felipe de Souza Leite, Srikar Vengallatore, Dilson E Rassier
KEY POINTS: When a skeletal muscle is stretched while it contracts, the muscle produces a relatively higher force than the force from an isometric contraction at the same length: a phenomenon referred to as residual force enhancement. Residual force enhancement is puzzling because it cannot be directly explained by the classical force-length relationship and the sliding filament theory of contraction, the main paradigms in the muscle field. We used custom-built instruments to measure residual force enhancement in skeletal myofibrils, and, for the first time, in cardiac myofibrils...
December 27, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27994045/effects-of-activation-on-the-elastic-properties-of-intact-soleus-muscles-with-a-deletion-in-titin
#15
Jenna A Monroy, Krysta L Powers, Cinnamon M Pace, Theodore Uyeno, Kiisa C Nishikawa
Titin has long been known to contribute to muscle passive tension. Recently, it was also demonstrated that titin-based stiffness increases upon Ca(2+)-activation of wildtype mouse psoas myofibrils stretched beyond overlap of the thick and thin filaments. In addition, this increase in titin-based stiffness upon activation was impaired in single psoas myofibrils from mdm mice with a deletion in titin. Here, we investigate the effects of muscle activation on elastic properties of intact soleus muscles from wildtype and mdm mice to determine whether titin may contribute to active muscle stiffness...
December 19, 2016: Journal of Experimental Biology
https://www.readbyqxmd.com/read/27991570/establishment-of-a-highly-sensitive-sandwich-elisa-for-the-n-terminal-fragment-of-titin-in-urine
#16
Nobuhiro Maruyama, Tsuyoshi Asai, Chiaki Abe, Akari Inada, Takeshi Kawauchi, Kazuya Miyashita, Masahiro Maeda, Masafumi Matsuo, Yo-Ichi Nabeshima
Muscle damage and loss of muscle mass are triggered by immobilization, loss of appetite, dystrophies and chronic wasting diseases. In addition, physical exercise causes muscle damage. In damaged muscle, the N-terminal and C-terminal regions of titin, a giant sarcomere protein, are cleaved by calpain-3, and the resulting fragments are excreted into the urine via glomerular filtration. Therefore, we considered titin fragments as promising candidates for reliable and non-invasive biomarkers of muscle injury. Here, we established a sandwich ELISA that can measure the titin N-terminal fragment over a biologically relevant range of concentrations, including those in urine samples from older, non-ambulatory Duchenne muscular dystrophy patients and from healthy donors under everyday life conditions and after exercise...
December 19, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27989621/binding-of-myomesin-to-obscurin-like-1-at-the-muscle-m-band-provides-a-strategy-for-isoform-specific-mechanical-protection
#17
Stefano Pernigo, Atsushi Fukuzawa, Amy E M Beedle, Mark Holt, Adam Round, Alessandro Pandini, Sergi Garcia-Manyes, Mathias Gautel, Roberto A Steiner
The sarcomeric cytoskeleton is a network of modular proteins that integrate mechanical and signaling roles. Obscurin, or its homolog obscurin-like-1, bridges the giant ruler titin and the myosin crosslinker myomesin at the M-band. Yet, the molecular mechanisms underlying the physical obscurin(-like-1):myomesin connection, important for mechanical integrity of the M-band, remained elusive. Here, using a combination of structural, cellular, and single-molecule force spectroscopy techniques, we decode the architectural and functional determinants defining the obscurin(-like-1):myomesin complex...
January 3, 2017: Structure
https://www.readbyqxmd.com/read/27986994/the-effects-of-a-skeletal-muscle-titin-mutation-on-walking-in-mice
#18
Cinnamon M Pace, Sarah Mortimer, Jenna A Monroy, Kiisa C Nishikawa
Titin contributes to sarcomere assembly, muscle signaling, and mechanical properties of muscle. The mdm mouse exhibits a small deletion in the titin gene resulting in dystrophic mutants and phenotypically normal heterozygotes. We examined the effects of this mutation on locomotion to assess how, and if, changes to muscle phenotype explain observed locomotor differences. Mutant mice are much smaller in size than their siblings and gait abnormalities may be driven by differences in limb proportions and/or by changes to muscle phenotype caused by the titin mutation...
December 16, 2016: Journal of Comparative Physiology. A, Neuroethology, Sensory, Neural, and Behavioral Physiology
https://www.readbyqxmd.com/read/27914791/aberrant-developmental-titin-splicing-and-dysregulated-sarcomere-length-in-thymosin-%C3%AE-4-knockout-mice
#19
Nicola Smart, Johannes Riegler, Cameron W Turtle, Craig A Lygate, Debra J McAndrew, Katja Gehmlich, Karina N Dubé, Anthony N Price, Vivek Muthurangu, Andrew M Taylor, Mark F Lythgoe, Charles Redwood, Paul R Riley
Sarcomere assembly is a highly orchestrated and dynamic process which adapts, during perinatal development, to accommodate growth of the heart. Sarcomeric components, including titin, undergo an isoform transition to adjust ventricular filling. Many sarcomeric genes have been implicated in congenital cardiomyopathies, such that understanding developmental sarcomere transitions will inform the aetiology and treatment. We sought to determine whether Thymosin β4 (Tβ4), a peptide that regulates the availability of actin monomers for polymerization in non-muscle cells, plays a role in sarcomere assembly during cardiac morphogenesis and influences adult cardiac function...
November 30, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27889803/reducing-rbm20-activity-improves-diastolic-dysfunction-and-cardiac-atrophy
#20
Florian Hinze, Christoph Dieterich, Michael H Radke, Henk Granzier, Michael Gotthardt
: Impaired diastolic filling is a main contributor to heart failure with preserved ejection fraction (HFpEF), a syndrome with increasing prevalence and no treatment. Both collagen and the giant sarcomeric protein titin determine diastolic function. Since titin's elastic properties can be adjusted physiologically, we evaluated titin-based stiffness as a therapeutic target. We adjusted RBM20-dependent cardiac isoform expression in the titin N2B knockout mouse with increased ventricular stiffness...
December 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
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