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https://www.readbyqxmd.com/read/28432215/actomyosin-based-tissue-folding-requires-a-multicellular-myosin-gradient
#1
Natalie C Heer, Pearson W Miller, Soline Chanet, Norbert Stoop, Jörn Dunkel, Adam C Martin
Tissue folding promotes three-dimensional (3D) form during development. In many cases, folding is associated with myosin accumulation at the apical surface of epithelial cells, as seen in the vertebrate neural tube and the Drosophila ventral furrow. This type of folding is characterized by constriction of apical cell surfaces, and the resulting cell shape change is thought to cause tissue folding. Here, we use quantitative microscopy to measure the pattern of transcription, signaling, myosin activation, and cell shape in the Drosophila mesoderm...
April 21, 2017: Development
https://www.readbyqxmd.com/read/28431892/a-humanized-hla-dr4-mouse-model-for-autoimmune-myocarditis
#2
M Emrah Şelli, Anita C Thomas, David C Wraith, Andrew C Newby
Myocarditis, the principal cause of dilated cardiomyopathy and heart failure in young adults, is associated with autoimmunity to human cardiac α-myosin (hCAM) and the DR4 allele of human major histocompatibility II (MHCII). We developed an hCAM-induced myocarditis model in human HLA-DR4 transgenic mice that lack all mouse MHCII genes, demonstrating that immunization for 3weeks significantly increased splenic T-cell proliferative responses and titres of IgG1 and IgG2c antibodies, abolished weight gain, provoked cardiac inflammation and significantly impaired cardiac output and fractional shortening, by echocardiography, compared to adjuvant-injected mice...
April 18, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28412087/pregestational-type-2-diabetes-mellitus-induces-cardiac-hypertrophy-in-the-murine-embryo-through-cardiac-remodeling-and-fibrosis
#3
Xue Lin, Penghua Yang, E Albert Reece, Peixin Yang
BACKGROUND: Cardiac hypertrophy is highly prevalent in patients with type 2 diabetes mellitus (T2DM). Experimental evidence has implied that pregnant women with T2DM and their children are at an increased risk of cardiovascular diseases. Our previous mouse model study has revealed that maternal T2DM induces structural heart defects in their offspring. OBJECTIVE: The present study aims to determine whether maternal T2DM induces embryonic heart hypertrophy in a murine model of diabetic embryopathy...
April 12, 2017: American Journal of Obstetrics and Gynecology
https://www.readbyqxmd.com/read/28407399/abnormal-rab11-rab8-vesicles-cluster-in-enterocytes-of-patients-with-microvillus-inclusion-disease
#4
Georg F Vogel, Andreas R Janecke, Iris M Krainer, Karin Gutleben, Barbara Witting, Sally G Mitton, Sahar Mansour, Antje Ballauff, Joseph T Roland, Amy C Engevik, Ernest Cutz, Thomas Müller, James R Goldenring, Lukas A Huber, Michael W Hess
Microvillus Inclusion Disease (MVID) is a congenital enteropathy characterized by accumulation of vesiculo-tubular endomembranes in the subapical cytoplasm of enterocytes, historically termed "secretory granules". However, neither their identity nor pathophysiological significance is well defined. Using immunoelectron microscopy and tomography we studied biopsies from MVID patients (3x Myosin 5b mutations, 1x Syntaxin3 mutation) and compared them to controls and genome-edited CaCo2 cell models, harboring relevant mutations...
April 13, 2017: Traffic
https://www.readbyqxmd.com/read/28406994/neisseria-gonorrhoeae-infects-the-human-endocervix-by-activating-non-muscle-myosin-ii-mediated-epithelial-exfoliation
#5
Liang-Chun Wang, Qian Yu, Vonetta Edwards, Brian Lin, Jessica Qiu, Jerrold R Turner, Daniel C Stein, Wenxia Song
Colonization and disruption of the epithelium is a major infection mechanism of mucosal pathogens. The epithelium counteracts infection by exfoliating damaged cells while maintaining the mucosal barrier function. The sexually transmitted bacterium Neisseria gonorrhoeae (GC) infects the female reproductive tract primarily from the endocervix, causing gonorrhea. However, the mechanism by which GC overcome the mucosal barrier remains elusive. Using a new human tissue model, we demonstrate that GC can penetrate into the human endocervix by inducing the exfoliation of columnar epithelial cells...
April 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28405145/acanthopanax-senticosus-polysaccharides-induced-intestinal-tight-junction-injury-alleviation-via-inhibition-of-nf-%C3%AE%C2%BAb-mlck-pathway-in-a-mouse-endotoxemia-model
#6
Jie Han, Ji-Hong Li, Guang Bai, Guo-Shun Shen, Jing Chen, Jia-Nan Liu, Shuo Wang, Xian-Jun Liu
AIM: To examine the effects of Acanthopanax senticosus polysaccharides (ASPS) on intestinal tight junction (TJ) disruption and nuclear factor-kappa B (NF-κB)/myosin light chain kinase (MLCK) activation in endotoxemia. METHODS: BALB/C mice (6-8-weeks-old) received continuous intragastric gavage of ASPS for 7 d before injection of lipopolysaccharide (LPS), or received ASPS once after LPS injection. Blood and intestinal mucosal samples were collected 6 h after LPS challenge...
March 28, 2017: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/28402887/the-closed-state-of-the-thin-filament-is-not-occupied-in-fully-activated-skeletal-muscle
#7
Sergey Y Bershitsky, Natalia A Koubassova, Michael A Ferenczi, Galina V Kopylova, Theyencheri Narayanan, Andrey K Tsaturyan
Muscle contraction is powered by actin-myosin interaction controlled by Ca(2+) via the regulatory proteins troponin (Tn) and tropomyosin (Tpm), which are associated with actin filaments. Tpm forms coiled-coil dimers, which assemble into a helical strand that runs along the whole ∼1 μm length of a thin filament. In the absence of Ca(2+), Tn that is tightly bound to Tpm binds actin and holds the Tpm strand in the blocked, or B, state, where Tpm shields actin from the binding of myosin heads. Ca(2+) binding to Tn releases the Tpm from actin so that it moves azimuthally around the filament axis to a closed, or C, state, where actin is partially available for weak binding of myosin heads...
April 11, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/28400443/plastin-increases-cortical-connectivity-to-facilitate-robust-polarization-and-timely-cytokinesis
#8
Wei Yung Ding, Hui Ting Ong, Yusuke Hara, Jantana Wongsantichon, Yusuke Toyama, Robert C Robinson, François Nédélec, Ronen Zaidel-Bar
The cell cortex is essential to maintain animal cell shape, and contractile forces generated within it by nonmuscle myosin II (NMY-2) drive cellular morphogenetic processes such as cytokinesis. The role of actin cross-linking proteins in cortical dynamics is still incompletely understood. Here, we show that the evolutionarily conserved actin bundling/cross-linking protein plastin is instrumental for the generation of potent cortical actomyosin contractility in the Caenorhabditis elegans zygote. PLST-1 was enriched in contractile structures and was required for effective coalescence of NMY-2 filaments into large contractile foci and for long-range coordinated contractility in the cortex...
April 11, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28400398/multi-imaging-method-to-assay-the-contractile-mechanical-output-of-micropatterned-human-ipsc-derived-cardiac-myocytes
#9
Alexandre J Ribeiro, Olivier Schwab, Mohammad A Mandegar, Yen-Sin Ang, Bruce R Conklin, Deepak Srivastava, Beth L Pruitt
Rationale: During each beat, cardiac myocytes generate the mechanical output necessary for heart function through contractile mechanisms that involve shortening of sarcomeres along myofibrils. Human induced pluripotent stem cells can be differentiated into cardiac myocytes that model cardiac contractile mechanical output more robustly when micropatterned into physiological shapes. Quantifying the mechanical output of these cells enables us to assay cardiac activity in a dish. Objective: We sought to develop a computational platform that integrates analytical approaches to quantify the mechanical output of single micropatterned cardiac myocytes from microscopy videos...
April 11, 2017: Circulation Research
https://www.readbyqxmd.com/read/28387646/unfair-competition-governs-the-interaction-of-pcpi-17-with-myosin-phosphatase-pp1-mypt1
#10
Joshua J Filter, Byron C Williams, Masumi Eto, David Shalloway, Michael L Goldberg
The small phosphoprotein pCPI-17 inhibits myosin light chain phosphatase (MLCP). Current models postulate that during muscle relaxation, phosphatases other than MLCP dephosphorylate and inactivate pCPI-17 to restore MLCP activity. We show here that such hypotheses are insufficient to account for the observed rapidity of pCPI-17 inactivation in mammalian smooth muscles. Instead, MCLP itself is the critical enzyme for pCPI-17 dephosphorylation. We call the mutual sequestration mechanism through which pCPI-17 and MLCP interact inhibition by unfair competition: MLCP protects pCPI-17 from other phosphatases, while pCPI-17 blocks other substrates from MLCP's active site...
April 7, 2017: ELife
https://www.readbyqxmd.com/read/28385814/tnf%C3%AE-enhances-force-generation-in-airway-smooth-muscle
#11
Murat Dogan, Young-Soo Han, Philippe F Delmotte, Gary C Sieck
Airway inflammation is a hallmark of asthma triggering airway smooth muscle (ASM) hyperreactivity and airway remodeling. TNFα increases both agonist-induced cytosolic Ca(2+) concentration and force in ASM. The effects of TNFα on ASM force may also be due to an increase in Ca(2+) sensitivity, cytoskeletal remodeling and/or changes in contractile protein content. We hypothesized that 24-h exposure TNFα increases ASM force by changing actin and myosin heavy chain (MyHC) content and/or polymerization. Porcine ASM strips were permeabilized with 10% Triton X-100, and force was measured in response to increasing concentrations of Ca(2+) (pCa 9...
April 6, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28379313/early-sensitization-of-myofilaments-to-ca2-prevents-genetically-linked-dilated-cardiomyopathy-in-mice
#12
Marco L Alves, Chad M Warren, Jillian N Simon, Robert D Gaffin, Eric M Montminy, David F Wieczorek, R John Solaro, Beata M Wolska
Background: : Dilated cardiomoypathies (DCM) are a heterogeneous group of inherited and acquired diseases characterized by decreased contractility and enlargement of cardiac chambers and a major cause of morbidity and mortality. Mice with Glu54Lys mutation in α-tropomyosin (Tm54) demonstrate typical DCM phenotype with reduced myofilament Ca 2+ sensitivity. We tested the hypothesis that early sensitization of the myofilaments to Ca 2+ in DCM can prevent the DCM phenotype. Methods and Results: To sensitize Tm54 myofilaments, we used a genetic approach and crossbred Tm54 mice with mice expressing slow skeletal troponin I (ssTnI) that sensitizes myofilaments to Ca 2+ ...
April 3, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28377413/quantifying-the-release-of-biomarkers-of-myocardial-necrosis-from-cardiac-myocytes-and-intact-myocardium
#13
Jack Marjot, Thomas E Kaier, Eva D Martin, Shiney S Reji, O'Neal Copeland, Mohammed Iqbal, Bob Goodson, Sarah Hamren, Sian E Harding, Michael S Marber
BACKGROUND: Myocardial infarction is diagnosed when biomarkers of cardiac necrosis exceed the 99th centile, although guidelines advocate even lower concentrations for early rule-out. We examined how many myocytes and how much myocardium these concentrations represent. We also examined if dietary troponin can confound the rule-out algorithm. METHODS: Individual rat cardiac myocytes, rat myocardium, ovine myocardium, or human myocardium were spiked into 400-μ L aliquots of human serum...
April 4, 2017: Clinical Chemistry
https://www.readbyqxmd.com/read/28371863/hypercontractile-mutant-of-ventricular-myosin-essential-light-chain-leads-to-disruption-of-sarcomeric-structure-and-function-and-results-in-restrictive-cardiomyopathy-in-mice
#14
Chen-Ching Yuan, Katarzyna Kazmierczak, Jingsheng Liang, Rosemeire Kanashiro-Takeuchi, Thomas C Irving, Aldrin V Gomes, Yihua Wang, Thomas P Burghardt, Danuta Szczesna-Cordary
Aims: The E143K (Glu→Lys) mutation in the myosin essential light chain (ELC) has been associated with restrictive cardiomyopathy (RCM) in humans, but the mechanisms that underlie the development of defective cardiac function are unknown. Using transgenic E143K-RCM mice, we sought to determine the molecular and cellular triggers of E143K-induced heart remodeling. Methods and Results: The E143K-induced abnormalities in cardiac function and morphology observed by echocardiography and invasive hemodynamics were paralleled by augmented active and passive tension measured in skinned papillary muscle fibers compared with wild-type (WT)-generated force...
March 23, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28366003/complete-characterization-of-cardiac-myosin-heavy-chain-223-kda-enabled-by-size-exclusion-chromatography-and-middle-down-mass-spectrometry
#15
Yutong Jin, Liming Wei, Wenxuan Cai, Ziqing Lin, Zhijie Wu, Ying Peng, Takushi Kohmoto, Richard L Moss, Ying Ge
Myosin heavy chain (MHC), the major component of myosin motor molecule, plays an essential role in force production during muscle contraction. However, a comprehensive analysis of MHC proteoforms arising from sequence variations and post-translational modifications (PTMs) remains challenging due to the difficulties in purifying MHC (~223 kDa) and achieving complete sequence coverage. Herein, we have established a strategy to effectively purify and comprehensively characterize MHC from heart tissue by combining size-exclusion chromatography (SEC) and middle-down mass spectrometry (MS)...
April 1, 2017: Analytical Chemistry
https://www.readbyqxmd.com/read/28363137/structures-related-to-attachment-and-motility-in-the-marine-eugregarine-cephaloidophora-cf-communis-apicomplexa
#16
Magdaléna Kováčiková, Timur G Simdyanov, Andrei Diakin, Andrea Valigurová
Gregarines represent a highly diversified group of ancestral apicomplexans, with various modes of locomotion and host-parasite interactions. The eugregarine parasite of the barnacle Balanus balanus, Cephaloidophora cf. communis, exhibits interesting organisation of its attachment apparatus along with unique motility modes. The pellicle covered gregarine is arranged into longitudinal epicytic folds. The epimerite is separated from the protomerite by a septum consisting of tubulin-rich filamentous structures and both are packed with microneme-like structures suggestive of their function in the production of adhesives important for attachment and secreted through the abundant epimerite pores...
March 7, 2017: European Journal of Protistology
https://www.readbyqxmd.com/read/28359939/tropomyosin-1-multiple-roles-in-the-developing-heart-and-in-the-formation-of-congenital-heart-defects
#17
Jennifer England, Javier Granados-Riveron, Luis Polo-Parada, Diji Kuriakose, Christopher Moore, J David Brook, Catrin S Rutland, Kerry Setchfield, Christopher Gell, Tushar K Ghosh, Frances Bu'Lock, Christopher Thornborough, Elisabeth Ehler, Siobhan Loughna
Tropomyosin 1 (TPM1) is an essential sarcomeric component, stabilising the thin filament and facilitating actin's interaction with myosin. A number of sarcomeric proteins, such as alpha myosin heavy chain, play crucial roles in cardiac development. Mutations in these genes have been linked to congenital heart defects (CHDs), occurring in approximately 1 in 145 live births. To date, TPM1 has not been associated with isolated CHDs. Analysis of 380 CHD cases revealed three novel mutations in the TPM1 gene; IVS1+2T>C, I130V, S229F and a polyadenylation signal site variant GATAAA/AATAAA...
March 27, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28356344/yap-promotes-myogenic-differentiation-via-the-mek5-erk5-pathway
#18
Ting-Huan Chen, Chen-Yu Chen, Hui-Chin Wen, Chia-Chu Chang, Horng-Dar Wang, Chih-Pin Chuu, Chung-Ho Chang
Yes-associated protein (YAP) is a transcriptional coactivator in the Hippo pathway that regulates cell proliferation, differentiation, and apoptosis. The MEK5/ERK5 MAPK cascade is essential for the early step of myogenesis. In this study, we generated C2C12 stable cell lines that expressed YAP (C2C12-YAP cells) and found that ERK5 and MEK5 were activated in C2C12-YAP cells compared with control C2C12 (C2C12-vector) cells. C2C12-YAP stable cells also differentiated into myotubes better than C2C12-vector cells, and expressed elevated levels of myogenin, a transcription factor that regulates myogenesis, as well as elevated levels of myosin heavy chain, a skeletal muscle marker...
March 29, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28348208/myo6-is-targeted-by-salmonella-virulence-effectors-to-trigger-pi3-kinase-signaling-and-pathogen-invasion-into-host-cells
#19
Andrew B E Brooks, Daniel Humphreys, Vikash Singh, Anthony C Davidson, Susan D Arden, Folma Buss, Vassilis Koronakis
To establish infections, Salmonella injects virulence effectors that hijack the host actin cytoskeleton and phosphoinositide signaling to drive pathogen invasion. How effectors reprogram the cytoskeleton network remains unclear. By reconstituting the activities of the Salmonella effector SopE, we recapitulated Rho GTPase-driven actin polymerization at model phospholipid membrane bilayers in cell-free extracts and identified the network of Rho-recruited cytoskeleton proteins. Knockdown of network components revealed a key role for myosin VI (MYO6) in Salmonella invasion...
April 11, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28345052/cardiac-myosin-binding-protein-c-ser-302-phosphorylation-regulates-cardiac-%C3%AE-adrenergic-reserve
#20
Ranganath Mamidi, Kenneth S Gresham, Jiayang Li, Julian E Stelzer
Phosphorylation of cardiac myosin binding protein-C (MyBP-C) modulates cardiac contractile function; however, the specific roles of individual serines (Ser) within the M-domain that are targets for β-adrenergic signaling are not known. Recently, we demonstrated that significant accelerations in in vivo pressure development following β-agonist infusion can occur in transgenic (TG) mouse hearts expressing phospho-ablated Ser(282) (that is, TG(S282A)) but not in hearts expressing phospho-ablation of all three serines [that is, Ser(273), Ser(282), and Ser(302) (TG(3SA))], suggesting an important modulatory role for other Ser residues...
March 2017: Science Advances
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