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Dissertations / Theses on the topic 'Contractile Proteins'

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Published: 4 June 2021
Last updated: 29 January 2023

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1

Bayliss, Christopher Richard. "Dysfunction of contractile proteins in hypertrophic cardiomyopathy." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9293.

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The contractility of human heart samples from patients diagnosed with hypertrophic cardiomyopathy were studied using a quantitative in vitro motility assay. The aim of this work was to investigate the molecular phenotype of thin filament proteins in the HCM heart. Three biopsy samples with thin filament mutations were studied alongside samples acquired from a subset of HCM patients classified with hypertrophic obstructive cardiomyopathy. The primary effect of thin filament mutations was investigated by reconstituting Factin with ACTC E99K into thin filament with donor troponin. The E99K actin filaments had a higher Ca2+-sensitivity then filaments composed of donor F-actin (with no mutation) (EC50 E99K/donor 0.78±0.14, p=0.02). A similar higher Ca2+- sensitivity was found when recombinant TnT K273N was incorporated into donor troponin and compared to native donor troponin (EC50 K273N/donor 0.54±0.17, p=0.006). Troponin was also purified from HOCM heart samples. This troponin did not contain a causative mutation but behaved abnormally in the response of thin filament Ca2+- sensitivity to changes in TnI phosphorylation (EC50 PKA-HOCM/HOCM 1.08±0.25, p=0.3) as mean TnI phosphorylation of PKA-HOCM was 1.56 molsPi/molsTnI and HOCM was 0.29 molsPi/molsTnI. Thus, thin filament Ca2+-sensitivity was uncoupled from TnI phosphorylation in thin filaments with HOCM troponin. When the native TnT subunits were replaced with recombinant TnT this coupling was restored (EC50 HOCM rTnT/HOCM 0.63±0.26, p=0.03). It would appear that the result of HCM-causing mutations are two-fold. The primary effect of the HCM-causing mutations is to increase thin filament Ca2+-sensitivity. However, the contraction machinery appears to be the target of secondary modifications, that occur due to the pathology of the disease. Resulting in further changes, such as changes in protein composition and post-translational modification. One major consequence of these modifications may be to uncouple the relatively labile regulation of thin filament Ca2+-sensitivity by TnI phosphorylation.
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2

Du, Fei. "A RabGAP protein and BEACH Family proteins regulate contractile vacuole formation and activity and chemotaxis in Dictyostelium." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3274747.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed Oct. 5, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 87-99).
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3

Stromme, Adrianna. "The characterization of the cytoskeleton and associated proteins in the formation of wound-induced contractile arrays /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116078.

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The cytoskeleton is an intrinsic aspect of all cells, and is essential for many cellular events including cell motility, endocytosis, cell division and wound healing. Remodeling of the cytoskeleton in response to these cellular activities leads to significant alterations in the morphology of the cell. One such alteration is the formation of an actomyosin contractile array required for cytokinesis, wound healing and embryonic development.
Cellular structure and shape depends upon tensional prestress brought about by the organization of cytoskeletal components. Using the Xenopus laevis oocyte wound healing model, it is first described how diminished cellular tension affects the balance of the Rho family of GTPases, and subsequently prevents the formation of actomyosin contractile arrays. This suggests that cellular tension in the cell is not created at the level of the cytoskeletal elements but rather via the upstream signaling molecules: RhoA and Cdc42.
The role of N-WASP (Neural-Wiscott Aldrich Syndrome Protein), a mediator of Arp2/3 based actin polymerization, is next examined for its putative role in cellular wound healing. Xenopus laevis oocytes injected with mutant N-WASP constructs reveals in vivo evidence that functional N-WASP is required for appropriate contractile array formation and wound closure.
Lastly, it is revealed that the cellular structures involved with single cell wound healing in other model systems are also important for the initial repair of severed muscle cells. Actin, non-muscle myosin-II, microtubules, sarcomeric myosin and Cdc42 are all recruited and reorganized at the edge of damaged C2C12 myotubes. This data promotes the possibility that an actomyosin array may be established in injured muscle cells as well.
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4

Bexis, Sotiria. "The relationship between vascular structure, contractile proteins, vascular reactivity and blood pressure in animal models of hypertension /." Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phb572.pdf.

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5

Llinares, Elisa. "Function, regulation and intracellular trafficking of the vacuolaryeast pq-loop (Ypq) proteins." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209704.

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The cytoplasm of eukaryotic cells contains several membrane-delimited compartments of specific molecular compositions and functions. Among those, the vacuole of fungal cells is often described as an organelle equivalent to the lysosomes of animal cells and the vacuoles of plant cells. These compartments indeed share two similar features: they contain a wide variety of hydrolases and are the most acidic compartments of the cell, which accounts for their key role in the intracellular degradation of macromolecules. In humans, dysfunctions of the lysosomes often give rise to lysosomal related diseases, such as lysosomal storage disorders. These are a class of metabolic disorders caused by the accumulation of non-degraded macromolecules or impaired export of hydrolytic degradation products. Cystinosis is an autosomal recessive disorder (1/200 000 incidence) generally associated with renal dysfunctions. It is caused by the accumulation and crystallization of cystine, the disulfide of cysteine, into the lumen of lysosomes. Cystinosin, the causative gene product of cystinosis, is present at the lysosomal membrane and catalyses the export of cystine from this compartment. The human cystinosin is a member of the Lysosomal Cystine Transporter (LCT) family. LCT proteins are conserved in all eukaryotic species and are defined by the presence of highly conserved PQ-loop motifs.

During this thesis work, we have studied three LCT proteins of the yeast Saccharomyces cerevisiae, named Ypq1, Ypq2 and Ypq3 (Yeast PQ-loop proteins 1, 2 and 3). We first showed that these proteins localize to the vacuolar membrane. We next studied the roles of these proteins, the regulation of their genes and the mechanisms and signals implicated in their delivery to the vacuolar membrane. We also contributed to the functional characterization of a mammalian homologue of yeast Ypq proteins, named rPqlc2.

In the first part of this work, we report that the Ypq proteins are most probably implicated in the export of basic amino acids from the vacuole to the cytosol. More precisely, Ypq2 and Ypq3 behave like vacuolar arginine and lysine exporters, respectively. Interestingly, the mammalian rPqlc2 protein expressed in yeast reaches the vacuolar membrane and functions as an orthologue of the Ypq proteins. Our results also reveal that the expression of the YPQ3 gene is regulated by the Lys14 transcription factor, responsible for the transcriptional activation of the LYS genes encoding enzymes implicated in the biosynthesis of lysine. We have also noted that, in general, the expression of the expression of the YPQ genes is regulated according to the quality of the nitrogen source available in the extracellular medium, eg. YPQ3 is sensitive to the nitrogen catabolite repression regulatory mechanism.

In the last part of this thesis work, we investigated the intracellular trafficking of the Ypq proteins and show that these predominantly reach the vacuolar membrane via the ALP (alkaline phosphatase) pathway due to the presence of a dileucine-based sorting signal in their sequences. Interestingly, a similar mechanism seems responsible for targeting to the yeast vacuole of the mammalian rPqlc2 protein.

Une caractéristique des cellules eucaryotes est leur organisation en compartiment internes délimité par une membrane lipidique, appelé organelles. Ces compartiments intracellulaires présentent une composition lipidique et protéique particulaire conforme à leur identité et fonction. Les lysosomes de cellules de mammifères et la vacuole fongique jouent un rôle clé dans la digestion intracellulaire de macromolécules et de ce fait leurs lumières sont enrichis d’enzymes hydrolytiques nécessaires à cette action. Des disfonctionnements du lysosome peuvent être la conséquence de pathologie chez l’homme, regroupé sous le nom de maladie lysosomale, lié à un à une accumulation de macromolécules non digéré ou un default d’export des produits d’hydrolysé depuis la lumière du lysosome. La cystinose est une maladie autosomale récessive avec une faible fréquence d’incidence (1/200 000) qui regroupe trois formes cliniques :deux formes rénales graves et une forme extra-rénale. Cette maladie est due à une accumulation et cristallisation de cystine dans la lumière du lysosome qui est corrélé à des mutations ponctuelles dans le gène CTNS qui code pour l’exporteur de cystine, la cystinosine. Cette protéine est un membre de la famille LCT (Lysosomal Cystine Transporter) qui possède des représentants chez les cellules animales, végétales et fongiques. Les protéines de la famille possèdent une taille et une topologie prédite similaire (7 segments transmembranaires) et on retrouve aussi au sein de ces protéines deux exemplaires de motifs PQ. Lors de ce travail de thèse nous nous sommes intéressés à trois membres de la famille LCT chez Saccharomyces cerevisiae que nous avons nommé Ypq1, Ypq2 et Ypq3 pour Yeast PQ-loop proteins. Ces protéines n’ayant pas fait l’objet de nombreuses études, nous nous sommes orientés vers une analyse fonctionnelle et transcriptionnelle. De plus, nous avons également étudié les mécanismes et signaux impliqué dans leur adressage vers la vacuole. Finalement, nous avons également inclus dans notre étude un homologue mammalien de ces protéines, rPqlc2.

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Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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6

Crampin, Helen. "The identification of a Spitzenkörper in 'C. albicans' and the partial characterisation of the contractile ring proteins." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425604.

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7

Willott, Ruth Heather. "Functional analyses of cardiomyopathic contractile proteins : mutations in troponin that cause familial hypertrophic cardiomyopathy and familial dilated cardiomyopathy." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400293.

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8

Bengreed, Amal H. I. "Characterisation of P2Y receptor-mediated contractile signalling and its regulation by G protein coupled receptor kinases and arrestin proteins in a rat bladder smooth muscle." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42795.

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ATP released from parasympathetic nerves can mediated bladder contraction, can activate purinergic P2Y/Gq/11-coupled G protein-coupled receptors (GPCR) expressed on detrusor (bladder) smooth muscle cells (DSMC). P2Y/Gq/11 signalling activates phospholipase C (PLC) and increases intracellular calcium concentrations to induce contraction. DSMC contractile GPCR activity is tightly regulated to prevent inappropriate contraction/incontinence. Additionally, GPCRs activity is regulated by G protein-coupled receptor kinase (GRK) and arrestin proteins, it is likely that they play a similar role in DSMC, and may help to maintain continence. Combining confocal imaging, calcium-sensitive dyes and selective P2X and P2Y receptor agonists/antagonists, showed that after 3-4 days in culture DSMC calcium signals were mediated by P2Y1 and P2Y2, but not P2X, P2Y4 or P2Y6 receptors. Repeated agonist additions indicated a desensitization of P2Y1 and P2Y2 activated phospholipase C (PLC)/Ca2+ signals, which was restored when the washout period between agonist challenges was increased. Transfection of DSMC with dominant-negative, catalytically inactive GRK mutants, which block endogenous GRK function, showed that P2Y1 and P2Y2 receptor stimulated calcium signalling was selectively regulated by GRK3 and GRK2, respectively. Furthermore, desensitization of P2Y1 and P2Y2 receptor PLC/Ca2+ was attenuated following RNAi-mediated knockdown of arrestin2 or arrestin3, suggesting both arrestins were able to regulate P2Y1/2 receptor signalling. To mimic the effects of obstructive bladder, DSMC were mechanically stretched which resulted in increased GRK2, and decreased GRK3/5/6 expression. These data show that DSMC express functional P2Y1/P2Y2 receptors which mediate purinergic agonist PLC/Ca2+ signalling, implying roles for P2Y1 and P2Y2 in bladder contraction and voiding. Furthermore, P2Y1 and P2Y2 receptor are selectively regulated by GRK and arrestin proteins, which suggests that GRK and arrestin proteins play an important role in the regulation of bladder tone. Furthermore, since GRK expression following mechanical stretch this may in turn affect GPCR signalling and produce dysregulation of DSMC contraction observed during incontinence.
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9

Johnsen, Lisa 1987. "Lipid droplet regulation by the differentially spliced proteins Osw5L and Osw5S." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/565566.

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Epithelial tissues undergo extensive remodeling during embryonic development. Recent studies have revealed that, in a number of developmental processes, epithelial remodeling is associated with pulsations of individual cell surface areas and cortical actomyosin flows. During Drosophila dorsal closure, the amnioserosa (AS), a contractile tissue covering the dorsal region of the embryo, shows contractile pulsations and regular actomyosin flows during the reduction of its apical surface area. The biophysical mechanism driving these shape pulsations as well as the role of contractile actomyosin waves in epithelial contraction and dorsal closure still remains unclear. In this project, we developed a biophysical model for cell shape oscillations that is based on intrinsic properties of the cell: cortex turnover, active contractility by force producing molecules and cell elasticity. We show that coupling these three key ingredients is sufficient for generating stable oscillations. Further, within this framework we were also able to generate waves by coupling the oscillating units and introducing a diffusion term to account for exchange of force producing molecules between the units. Next, we investigated the role for these contractile actomyosin waves in tissue remodeling. We developed a novel technique that allowed us to apply mechanical stretch on the AS tissue and study the response of cells to such stress. With this method, we were able to arrest the pulsatile contractions and actomyosin flows in AS cells. We show that this arrest is associated with the relocalisation of actin and myosin from the medial region of the cells towards the adherens junctions to maintain junction integrity upon stretch. This relocalisation of myosin directly correlates with the junctional strain and does not occur in cells that have excessive membrane material as a consequence of endocytosis inhibition. In the latter case, cells continue pulsing and seem to be “insensitive” to stretch. Upon stretch release, myosin relocalises to the medial area of the cell and pulsations resume. This indicates that cells can switch between two states depending on tension: one in which cells exhibit shape oscillations associated with contractile actomyosin pulses and waves, and the other where cell shape is stabilised with myosin preferentially localised at the cell junctions. Further, following release from long duration ( >10mins ) stretch application, cell junctions were highly wrinkled. Strong and consistent localisation of myosin waves at these regions led to straightening and reduction of junctional lengths. Moreover, during dorsal closure, AS cells constantly reduce their areas while maintaining junctions of consistent thickness and length relative to area. This is not the case where endocytosis is blocked or myosin activity is down-regulated. Our results not only shed light on fundamental physical properties of the actomyosin cortex, in particular they also indicate a role of myosin contractile waves in junctional remodeling during AS cell constriction.
Los tejidos epiteliales llevan a cabo una remodelación extensiva durante el desarrollo embrionario. Estudios recientes han revelada que, en un sinnumero de procesos de desarrollo embrionario, la remodelación epitelial se asocia con pulsaciones de áreas en células individuales y con flujos corticales de actomiosina. Durante el cierre dorsal de Drosophila, la amnioserosa (AS), un tejido contractil que cubre la región dorsal del embrión, se observan pulsaciones contráctiles en células individuales y flujos regulares de actomiosina durante la reducción de la superficial apical celular. Al día de hoy, no se conoce el mecanismo biofísico que produce estas pulsaciones celulares ni y el papel que tienen las oscilaciones contráctiles de actomiosina en el epitelio del cierre dorsal embrionario. En este proyecto, se desarrolló un modelo biofísico para entender estas oscilaciones celulares. El modelo se basa en propiedades intrínsecas de la célula como la rotación de la corteza celular, la contractilidad activa mediante moléculas productoras de fuerza y la elasticidad celular. Utilizando éste modelo, se muestra que acoplando estas tres propiedades clave es suficiente para generar oscilaciones celulares estables. Además, dentro de este marco, se han generado oscilaciones mediante el acoplamiento de varias unidades oscilantes y la introducción de un término de difusión para considerar el intercambio de moléculas productoras de fuerza entre las unidades. A continuación, se investigó el papel de estas oscilaciones contráctiles de actomiosina en la remodelación de tejidos. Como resultado, se desarrolla una técnica innovadora que permite aplicar extensión mecánica al tejido de AS y estudiar la respuesta celular ante tal estrés. Con este método, se pueden detener las pulsaciones contráctiles y los flujos de actomiosina en células de la AS. Se muestra que este arresto celular está asociado con la relocalización de actina y miosina de la región central de las células hacia las uniones adherentes intercelulares para mantener su integridad durante la extension epitelial. Esta relocalización de miosina se correlaciona directamente con la tensión en uniones intercelulares y no ocurre en células en las que el reciclaje cellular a través de endocitosis se ha bloqueado. El resultado es un exceso en la acumulación de membrana plasmática en células oscilantes que no responden a la extension epitelial. Tras liberar al tejido de la extension epithelial, la miosina se relocaliza a la área central de las células y las pulsaciones continuan. Esto indica que las células pueden cambiar entre dos estados según la tension aplicada: uno dónde las células muestran oscilaciones asociadas con pulsaciones contráctiles de actomiosina, y otra donde la forma celular se establece con la localización preferente de miosina en las uniones intercelulares. Además, tras liberar el tejido de una extensión de alta duración (>10mins), las uniones intercelulares sufrieron corrugaciones. La localización consistente de oscilaciones de miosina en las regions corrugadas, resulta en una extension y reducción en la longitud de las uniones intercelulares. Además, durante el cierre dorsal, las células de la AS reducen sus areas constantemente, mientras mantienen uniones intercelulares de espesor consistente y longitud relativa a su área. Esto no es el caso cuando la endocitosis se bloquea o la actividad de miosina se reduce. Nuestros resultados no solo muestran las propiedades fundamentales de la corteza cellular de actomiosina, también indican el papel de oscilaciones contráctiles de miosina en la remodelación de uniones intercelulares durante la constricción de la AS.
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10

Sjuve, Rolf. "Function of contractile and cytoskeletal proteins in smooth muscle effects of hypertrophy and age and of desmin removal in a transgenic animal /." Lund : Dept. of Physiology and Neuroscience, Lund University, 1998. http://books.google.com/books?id=ccFqAAAAMAAJ.

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11

Herron, Todd J. "Molecular regulation of power output in single rat skinned cardiac myocytes." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3052177.

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12

Amorin, Vanessa Almeida. "Remodelamento das proteínas contráteis cardíacas na transição da hipertrofia compensada para falência cardíaca." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17143/tde-26042018-164257/.

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A sobrecarga crônica de pressão causa hipertrofia, disfunção e insuficiência cardíaca (IC). O mecanismo envolvido na transição da hipertrofia cardíaca compensada para descompensada ainda não é totalmente entendido. Evidências sugerem que modificações nas proteínas contráteis poderiam contribuir para disfunção contrátil e evolução para IC. Neste sentido, estudos mostraram mudanças na expressão das proteínas da maquinaria contrátil durante o desenvolvimento da doença cardíaca como um mecanismo inicialmente benéfico. Porém, na insuficiência cardíaca, ocorrem alterações estruturais que prejudicam a contratilidade. Contudo, não se sabe ao certo quais proteínas estariam contribuindo para a transição da hipertrofia compensada para a insuficiência cardíaca. Este estudo teve como objetivo investigar as alterações das proteínas da maquinaria contrátil na transição da hipertrofia cardíaca compensada para descompensada e correlacionar essas alterações com a função cardíaca. Ratos Wistar machos foram submetidos a estenose da aorta abdominal. Após 90d da cirurgia, foram realizados ecocardiograma, análise da pressão sanguínea e os corações foram coletados para realização do Western blot e imunofluorescência para miosina de cadeia pesada, actina sarcomérica, troponina T e troponina I. Os dados foram considerados significantes quando p<0,05. Aos 90d, 70,0±5,35% dos animais apresentaram hipertrofia cardíaca (HH) e 30,3±4,79% corações hipertrofiados+dilatados (HD). A pressão arterial média aumentou 58,2% no HH e 55,0% no HD. As? expressões? de? ?-actina sarcomérica, miosina de cadeia pesada, troponina T e I aumentaram no grupo HH. No grupo HD, a miosina de cadeia pesada e a troponina T reduziram significantemente. A função sistólica manteve-se preservada nos grupos controle e HH, porém reduzida no HD. A perda estrutural da miosina de cadeia pesada e da troponina T poderia contribuir para a insuficiência cardíaca observada nesse modelo experimental.
Hypertension causes hypertrophy, cardiac dysfunction and heart failure (HF). The mechanisms implicated in the transition from compensated to decompensated cardiac hypertrophy are not fully understood. There is considerable evidence that changes in the contractile proteins may contribute to the contractile dysfunction and progression to HF. Studies have shown changes in the expression of contractile proteins during the development of heart disease as a mechanism that is initially beneficial. However, in heart failure there is an intrinsic reduction of cross-bridges that contributes to impaired contractility. It is not known which proteins are contributing to the transition from compensated hypertrophy to heart failure. We investigated ?-sarcomeric actin, heavy chain myosin and troponins T and I in the transition from compensated to decompensated cardiac hypertrophy and correlate these alterations with cardiac function. Male Wistar rats were submitted to abdominal aorta constriction and killed at 90 days post-surgery (dps). The hearts were collected; Western blot and immunofluorescence were performed to investigate ?-sarcomeric actin, heavy chain myosin and troponins T and I. Blood pressure and cardiac systolic function were evaluated. Data were considered significant when p<0.05. At 90 dps, 70,0±5,35% presented hypertrophic hearts (HH) and 30,3±4,79% hypertrophic+dilated hearts (HD). Mean blood pressure increased 58.19% in HH and 54.96% in HD. Heavy chain myosin, troponin T, troponin I and ?-sarcomeric actin expression increased in HH. In HD, only heavy chain myosin and troponin T reduced significantly. The systolic function was the same in control and HH animals and reduced in HD. The structural loss of heavy chain myosin and troponin T could contribute to heart failure observed in this experimental model of abdominal aorta constriction.
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McCloskey, Diana Teresa. "Adrenergic regulation of cardiac muscle contraction and relaxation." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324975.

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Betters, Jenna Leigh Jones. "Trolox supplementation during mechanical ventilation attenuates contractile dysfunction and protein degradation." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0004290.

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Coue, Martine. "Etude des effets de deux proteines associees a l'actine sur la polymerisation de l'actine." Paris 6, 1987. http://www.theses.fr/1987PA066318.

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L'etude des effets de deux proteines du serum, la gelsoline et de la proteine de liaison de la vitamine sur la polymerisation de l'actine a permis d'obtenir des informations: 1) sur le mecanisme d'action d'une proteine qui se fixe a un bout des filaments et qui les coupe et aussi d'une proteine qui se fixe uniquement au monomere d'actine 2) sur le mecanisme de la polymerisation au bout pointu des filaments d'actine. Ces resultats permettent de mieux envisager le role de la gelsoliune et la proteine de liaison de la vitamine d dans le serum
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Lin, Tsai Jing Eric. "Distribution of excitation-contraction coupling proteins as a function of development." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/20563.

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Excitation-contraction (EC) coupling in the neonatal rabbit heart has been previously shown to be mediated predominately by reverse-mode activity of the sodium-calcium exchanger (NCX). Thus the regulation of NCX is a primary determinant of neonatal cardiac contractility. It is proposed that in neonate hearts, a restricted domain allows a sodium current (INa) to mediate a large elevation in subsarcolemmal sodium concentration which then drives calcium entry through reverse-mode NCX. Functional data suggest that calcium influx through NCX can also trigger calcium induced calcium release (CICR). Traditionally, neonatal myocytes are thought to mediate EC coupling exclusively through trans-sarcolemma calcium influx. This model of EC coupling is distinct from the adult model of EC coupling in that it does not involve a significant CICR component. Traditionally, CICR processes are thought to be a hallmark of adult EC coupling processes where CICR is triggered exclusively by the L-type calcium current. Neonatal myocytes were previously believed to be too immature to sustain physiologically significant levels of CICR. Yet recent functional data suggest that not only are neonatal myocytes able to sustain CICR but that neonatal myocytes trigger CICR independently of the calcium current. Neonatal myocytes appear to trigger CICR exclusively though reverse-mode NCX activity (NCX-CICR). The phenomenon of NCX-CICR, prominent in early developmental stages and declining with further development, suggest that the neonatal myocardium contains specialized microdomains that allow NCX-CICR to occur. To investigate this unique EC coupling phenotype, three-dimensional confocal microscopy and advanced digital image analysis techniques are utilized to quantify the presence of these specialized microdomains and to determine the changes in these microdomains that occur with development.
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Tanner, Bertrand Clarke William. "Spatial coupling between sarcomeric proteins controls Ca2+-sensitive contraction muscle : a complementary research approach integrating theory with experiments /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/7995.

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Morgan, Matthew James. "The investigation of aspects of contractile protein gene expression with in rat skeletal muscle." Thesis, Royal Veterinary College (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300249.

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19

Schuster, Joseph M. "The contribution of titin to striated muscle shortening." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/5758.

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Thesis (M.S.)--University of Missouri-Columbia, 2008.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "December 2008" Includes bibliographical references.
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DAVID, CHRISTINE. "Caracterisation d'une proteine de type centrine, associee aux myonemes contractiles des cilies entodiniomorphes." Clermont-Ferrand 2, 1993. http://www.theses.fr/1993CLF21580.

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Les myonemes sont des reseaux de filaments fins (3-6 nm de diametre), pouvant induire des contractions calcium-dependantes, d'une partie ou de la totalite du corps cellulaire de nombreux protistes. Dans ce travail, nous avons caracterise une proteine fixatrice d'ions calcium, qui pourrait jouer un role essentiel dans la contraction des myonemes, chez les cilies entodiniomorphes. Cette proteine que nous avons appelee calmyonemine, est immunologiquement apparentee aux centrines, avec lesquelles elle partage un grand nombre de proprietes biochimiques: faible poids moleculaire, point isoelectrique acide, sites de fixation du calcium de type ef-hand, modification conformationnelle calcium-dependante. Un microsequencage de la calmyonemine, a mis en evidence de tres fortes identites de sequence avec la centrine de chlamydomonas, et dans une moindre mesure, avec les autres proteines ayant des domaines ef-hand. La calmyonemine ainsi caracterisee, a ete localisee par immunofluorescence, au niveau de divers myonemes, situes aux extremites des levres circumciliaires, sous la ciliature apicale, le long de l'sophage, et autour du cytoprocte. La dynamique de ces differents reseaux, a ete egalement suivie au cours de la morphogenese de division. De plus, nous avons montre que la calmyonemine des entodiniomorphes, est impliquee dans le comportement cyto-alimentaire, et dans la retraction des zones ciliaires en reponse a un stress environnemental. Des resultats preliminaires de purification de la proteine au moyen de techniques chromatographiques, sont egalement rapportes
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21

Boppart, Marni D. "Regulation of stress-activated protein kinases by exercise and contraction in skeletal muscle." Thesis, Boston University, 2000. https://hdl.handle.net/2144/36769.

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Thesis (Sc.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The c-Jun NH2-terminal kinase (JNK) and p38 intracellular signaling cascades are mitogen-activated protein kinase (MAPK) signaling pathways that are activated in mammalian cells by a variety of stressors, including proinflammatory cytokines, osmotic shock, and shear stress. The purpose of this dissertation research was to examine the effect of injury-producing exercise on JNK and p38 activities in human skeletal muscle and to determine whether mechanical stress is a primary stimulator of JNK and p38 activities with contraction. Twelve healthy subjects (7M/5F) completed maximal concentric or eccentric knee extensions on an isokinetic dynamometer (10 sets, 10 reps). Needle biopsies were obtained from the vastus lateralis muscle 24 h before exercise, immediately post-exercise, and 6 h post-exercise. While both forms of exercise increased JNK activity immediately post-exercise, eccentric contractions resulted in a much higher activation (15-fold vs. 4-fold increase above basal for eccentric and concentric, respectively). By 6 h post-exercise, JNK activity decreased back to baseline values. In a separate study, 14 male subjects completed a 42.2 km marathon. Biopsies were obtained from the vastus lateralis muscle 10 days prior to the marathon, immediately following the race, and 1, 3, and 5 days after the race. JNK activity increased 7-fold over basal immediately postexercise, but decreased back to basal 1, 3, and 5 days after the exercise. The activity of p38y also was increased and decreased in a similar pattern. However, no regulation was observed for p38α. In a third study, the effects of contraction and static stretch on JNK activity and p38 phosphorylation were determined in the rat soleus muscle in vitro. Static stretch dramatically increased JNK activity and p38 phosphorylation, whereas isometric contraction resulted in much smaller increases in JNK activity and p38 phosphorylation. The regulation of focal adhesion proteins also was examined following both exercise and contraction. The work presented in this thesis demonstrates that injury-producing exercise results in the marked activation of the JNK and p38 stress-activated protein kinases and provides evidence that mechanical stress may be a major contributor to increases in JNK and p38 activities observed following contraction in rat and human skeletal muscle.
2031-01-01
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22

Zoued, Abdelrahim. "Biogenesis and membrane anchoring of the Type VI secretion contractile tail." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM4090.

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Récemment, le système de sécrétion de type VI (SST6) a été identifié comme un nouvel acteur clé dans la compétition inter-bactérienne parmi le large arsenal dont dispose les bactéries. L’une des particularités du SST6 est de cibler à la fois des cellules eucaryotes et procaryotes. Le T6SS est un complexe protéique formé par l’assemblage de deux ‘sous-complexes’. Le premier sert à l’ancrage de la machinerie au sein de l’enveloppe bactérienne et le second agit comme une arbalète moléculaire. Le mécanisme d’action du SST6 est très similaire à celui d’autres machineries contractiles telles que celui des bactériophages : la contraction d’un fourreau propulse une flèche, composée d’un tube avec une aiguille à son extrémité, directement dans la cellule cible afin de délivrer les différentes toxines. Mon projet de thèse consiste à comprendre quelles sont la structure et la biogénèse des deux différents complexes et de comprendre comment ils sont assemblés. Nous utilisons comme modèle la bactérie pathogène à Gram négatif Escherichia coli entéroagrégative. J’ai pu démontrer que le complexe membranaire est assemblé en premier, avec l’adressage de la lipoprotéine de membrane externe TssJ, puis le recrutement séquentiel de TssM et TssL, deux protéines de membrane interne. Le complexe membranaire recrute ensuite une plateforme d’assemblage, appelée ‘baseplate’. Nous avons identifié et caractérisé les composants de cette ‘baseplate’ qui sert de plateforme d’assemblage pour le recrutement du reste de la machinerie (fourreau et flèche). Enfin, nous avons identifié et déterminé le rôle de la protéine TssA, une protéine qui coordonne la polymérisation du fourreau et de la flèche
Among the broad weaponry of bacteria, the recently identified type VI secretion system (T6SS) emerges as one of the key player in bacterial competition. T6SS is a versatile machinery that targets both eukaryotic and prokaryotic cells. This molecular weapon assembles two evolutionarily different sub-assemblies. One complex anchors the machinery to the cell envelope while the second acts as a molecular crossbow. The mechanism of action of the T6SS is similar to other known contractile machineries such as bacteriophages: the contraction of a sheath propels an arrow, constituted of a tail tube capped by a cell-puncturing device, directly into the prey cell to deliver effector toxins. My Ph.D project was to provide mechanistic details on the structure and biogenesis of the two T6SS sub-complexes and to understand how they are connected, using entero-aggregative Escherichia coli as model bacterium. I have demonstrated that the membrane complex is assembled first and starts with the positioning of the outer membrane TssJ lipoprotein and proceeds inward, from the outer to the inner membrane, through the sequential recruitment of the TssM and TssL subunits. After assembly, the membrane complex recruits an assembly platform called the baseplate. We identified and characterized the components of this baseplate, which serves as assembly platform for the tail. We further demonstrated that the functional and physical interaction between the T6SS membrane complex and the baseplate is mediated by multiple contacts. Finally, we identified and deciphered the role of TssA, a protein that coordinates the polymerizations of the tail tube and sheath
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23

van, Wieringen Tijs. "Intra- and Extracellular Modulation of Integrin-directed Connective Tissue Cell Contraction." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-102349.

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All blood vessels in the microvasculature are embedded in loose connective tissue, which regulates the transport of fluid to and from tissues. The intersti-tial fluid pressure (IFP) is one of the forces that control this transport. A lowering of IFP in vivo results in an increased transport of fluid from the circulation into the underhydrated connective tissues, resulting in edema formation. During homeostasis, contractile connective tissue cells exert a tension on the connective tissue fibrous network by binding with β1 in-tegrins, thereby actively controlling IFP. During inflammation, the IFP is lowered but platelet-derived growth factor (PDGF)-BB induces an IFP nor-malization dependent on integrin αVβ3. We demonstrate that extracellular proteins from Streptococcus equi subspecies equi modulated cell-mediated and integrin αVβ3-directed collagen gel contraction in vitro. One of these proteins, the collagen- and fibronectin binding FNE, stimulated contraction by a process dependent on fibronectin synthesis. This study identified a pos-sible novel virulence mechanism for bacteria based on the ability of bacteria to modulate the edema response. Another protein, the collagen-binding pro-tein CNE, inhibited contraction and this led to the identification of sites in collagen monomers that potentially are involved in connecting αVβ3 to the collagen network. PDGF-BB and prostaglandin E1 (PGE1) stimulate and inhibit collagen gel contraction in vitro and normalize and lower IFP, respec-tively. We showed that these agents affected both similar and different sets of actin-binding proteins. PDGF-BB stimulated actin cytoskeleton dynamics whereas PGE1 inhibited processes dependent on cytoskeletal motor and adhesive functions, suggesting that these different activities may partly ex-plain the contrasting effects of PGE1 and PDGF-BB on contraction and IFP. Mutation of the phosphatidylinositol 3’-kinase (PI3K), but not phospholipase C (PLC)γ activation site, rendered cells unable to respond to PDGF-BB in contraction and in activation of the actin binding and severing protein cofilin. Ability to activate cofilin after PDGF-BB stimulation correlated with ability to respond to PDGF-BB in contraction, suggesting a role for cofilin in this process downstream of PDGF receptor-activated PI3K. Many proteins can modulate contraction either by affecting the extracellular matrix and cell adhesions or by altering cytoskeletal dynamics. Knowledge on how these proteins might influence IFP is likely to be of clinical importance for treat-ment of inflammatory conditions including anaphylaxis, septic shock and also carcinoma growth.
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KACEMI, ABDELKRIM. "Caracterisation des proteines contractiles et culture des cellules des microvaisseaux ftaux du placenta humain." Paris 6, 1995. http://www.theses.fr/1995PA066632.

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Le placenta humain est richement irrigue et ses fonctions dependent essentiellement de sa vascularisation. Neanmoins, la physiopathologie des cellules vasculaires et perivasculaires de la circulation ftale intraplacentaire a ete peu etudiee. Dans cette etude, nous avons examine la repartition des proteines contractiles et la proportion de leurs differentes isoformes dans les vaisseaux ombilico-placentaires issus de grossesses normales. Nous avons ensuite realise l'isolement et la culture des cellules perivasculaires (cellules endotheliales et pericytes) provenant de microvaisseaux ftaux intraplacentaires. Des differences majeures ont ete observees dans la composition en isoformes des proteines contractiles des vaisseaux preplacentaires et intraplacentaires. Contrairement aux vaisseaux preplacentaires, qui renferment surtout des isoformes musculaires, les vaisseaux villositaires possedent principalement des isoformes non musculaires de l'actine et de la myosine. Les cellules endotheliales des microvaisseaux placentaires que nous avons isolees par digestion enzymatique puis cultivees sur matrice de gelatine, satisfont aux principaux criteres classiques de caracterisation immunocytochimique. Elles incorporent en particulier les lipoproteines acetylees et elles reagissent positivement a l'anticorps anti-von willebrand. Les pericytes ont ete isoles et cultives a partir d'explants microvasculaires, puis caracterises par un anticorps anti- -actine de type musculaire lisse. En culture avec les cellules endotheliales, ils donnent naissance a des nodules mixtes endothelio-pericytaires. Differentes applications physiopathologiques de ces methodes de culture peuvent etre envisagees: l'etude en monocouches de la permeabilite capillaire placentaire, celle de la repartition des isoformes des proteines contractiles dans le cas d'hypertension gravidique ou du retard de croissance intra-uterin et l'analyse en co-culture des phenomenes de vasculogenese
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25

Besse, Sophie. "Le coeur senescent normal et hypertendu : mecanique et energetique cardiaques, proteines contractiles et fibrose." Paris 11, 1993. http://www.theses.fr/1993PA112300.

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La senescence induit des modifications des proprietes contractiles du muscle papillaire gauche isole de rat qui sont associees a des modifications de l'expression des genes codant pour les proteines contractiles: diminution de la vitesse de raccourcissement a charge nulle (vmax) correlee a un changement de l'expression des genes codant pour les chaines lourdes de la myosine, diminution de la vitesse de reelongation correlee a une diminution de l'expression du gene codant pour la ca#2#+ atpase du rs et prolongation de la contraction isotonique et isometrique. De plus, la courbure g de l'hyperbole force-vitesse de hill est augmentee et le taux de recyclage des ponts actine-myosine est ralenti. Un tel processus d'adaptation conduit a une amelioration de l'efficacite de la contraction et l'ensemble de ces modifications indique une coordination etroite entre les processus d'excitation, de contraction et de relaxation. L'expression des genes codant pour le recepteur beta1 adrenergique et la sous unite alpha de la proteine gs est egalement alteree au cours du vieillissement et ces modifications sont probablement impliquees dans la diminution de reponse contractile a l'exercice et/ou aux agonistes beta-adrenergiques. Enfin, la senescence est associee a une alteration de la tension active developpee et a des troubles du rythme majeurs probablement tous deux lies a la presence importante de fibrose. Les contenus relatifs en arnm des collagenes type i et iii sont severement diminues alors que la concentration en hydroxyproline est augmentee considerablement. Cette dissociation entre le contenu en arnm et en proteine indique une regulation complexe de la synthese de collagene au cours du vieillissement impliquant des processus traductionnels et/ou post-traductionnels. En reponse a une hypertension induite par un traitement aux mineralocorticoides+sel (doca-sel), le cur age a garde la capacite de s'hypertrophier et d'adapter sa fonction contractile de la meme facon qu'un cur jeune soumis a la meme surcharge. Cependant, un tel traitement n'induit pas de fibrose et de troubles du rythme supplementaires et l'expression des genes codant pour les collagenes type i et iii n'est pas modifiee. Il semble donc que la reponse fibrotique du cur age a une hypertension aux mineralocorticoides soit diminuee
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26

Singh, Kulpreet. "Restoration of Contractile Protein Expression and Colonic Smooth Muscle Function by Hydrogen Sulfide in DMD Mice." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5790.

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Duchenne Muscular Dystrophy (DMD), characterized by the lack of dystrophin, results from a mutation in the Xp21 gene which encodes for the protein dystrophin that links the extracellular matrix to the actin cytoskeleton in skeletal, cardiac and smooth muscle. Slow colonic transit and chronic constipation are common in DMD patients due to the weakening of the abdominal wall muscles and gut smooth muscle. However, the cause of this hypocontractility in DMD patients and the expression of contractile proteins in smooth muscle are unknown. Expression of contractile proteins is regulated by the signaling pathways activated by excitatory (e.g., acetylcholine, ACh) and inhibitory transmitters (e.g., nitric oxide). Hydrogen sulfide (H2S) is well-known for its anti-oxidant effects; however, its utility to restore DMD-induced effects is unknown. Aim: To investigate the expression of contractile proteins and smooth muscle function in the colon of wild type mice and models of DMD (mdx and mdx/mTR mice) and the effect of H2S on these in mdx mice. Methods: Contraction of colonic segments was measured in the longitudinal orientation from 3-month old control and mdx mice, and 9-month old control and mdx/mTR mice, (mdx/mTR exhibit increased disease severity). The effect of SG1002, an orally active slow releasing H2S agent, was tested in mdx/mTR mice (40 mg/kg body weight in chow/every 3 days starting from 3 weeks to 9 months). Expression of contractile proteins was measured by qRT-PCR and western blot. Results: Expression of smoothelin, caldesmon, calponin and tropomyosin was decreased in colonic smooth muscle of mdx mice compared to control. This decrease was associated with a decrease in ACh-induced contraction in colonic segments (21 ± 3 mN/100 mg tissue in control and 3 ± 1 mN/100 mg tissue in mdx mice). To identify the specific involvement of smooth muscle dysfunction in the decrease in contraction, colonic muscle cells were isolated and contraction in response to ACh was measured by scanning micrometry and expressed as the percent decrease in cell length from control cell length. ACh-induced contraction was also inhibited in muscle cells isolated from mdx mice compared to control (43±5% in control and 27±3% in mdx mice). ACh-induced contraction was decreased in colonic segments from mdx/mTR mice (12 ± 2 mN/100 mg tissue in control versus 4 ± 1 mN/100 mg tissue in mdx/mTR) and the decrease was partly reversed by SG1002 treatment (9 ± 1 mN/100 mg tissue). mRNA expression of thin filament associated proteins was also decreased in colonic smooth muscle from mdx/mTR mice and the decrease was reversed by SG1002. These results suggest that H2S restores contractile protein mRNA expression and contraction in mdx/mTR mice. Conclusion: The data indicate that the lack of dystrophin in mdx mice adversely affects colonic smooth muscle contractility through the down regulation of contractile protein mRNA expression. Treatment of mdx/mTR mice with H2S restores contractile phenotype. Thus, H2S treatment would be an area of study in therapeutic control of DMD-induced gastrointestinal motility disorders.
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Round, Elaine Kay. "Identification and analysis of G-protein pathway control in the Caenorhabditis elegans defecation motor program /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10283.

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28

Waters, Carrie Baird. "Involvement of tyrosine kinases in endothelin-1-induced contraction of porcine coronary arteries /." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9946309.

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29

Norman, Catalina. "Influence of the thin filament calcium activation on muscle force production and rate of contraction in cardiac muscle." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1178751966.

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30

Waters, Carrie B. "Involvement of tyrosine kinases in endothelin-1-induced contraction of porcine coronary arteries." free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9946309.

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31

Glund, Stephan. "Molecular mechanisms governing contraction-induced metabolic responses and skeletal muscle reprogramming /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-436-5/.

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32

Redwood, Charles Stuart. "Identification of the functional domains of smooth muscle caldesmon." Thesis, Imperial College London, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243858.

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33

Janes, Daniel Peter. "Structural and functional approaches to myosin linked regulation using expressed protein fragments." Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249481.

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34

Saban, Melissa. "The effect of extracellular matrix on airway smooth muscle cell contractile protein expression and calcium response to serotonin." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103604.

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The asthmatic airway wall is characterized by airway remodeling, including changes in the extracellular matrix (ECM) and increased airway smooth muscle (ASM) cell mass. Further, asthmatic ASM has been shown to demonstrate enhanced contractility. Recently, we and others have shown that alterations in the matrix upon which ASM cells are grown in culture, can affect the degree of ASM cell proliferation and apoptosis. Whether changes in matrix can affect ASM cell contractility is less clear. ASM cells were isolated from the trachea of Brown Norway (BN) rats sensitized subcutaneously with ovalbumin (OVA) and challenged with either OVA or saline (SAL) as a control. Cells were grown in culture on plastic as a control, or on plates previously coated with collagen I (col), decorin (dcn) or biglycan (bgn). Contractile protein expression as well as single cell Ca2+ responses to serotonin was measured. Both SAL and OVA ASM cells grown on col had a significant reduction in α-smooth muscle actin (α-SMA) and calponin content. A significant increase in α-SMA and calponin was observed in OVA ASM cells grown on bgn but not in SAL cells. Dcn did not significantly affect α-SMA or calponin in SAL or OVA cells. Ca2+ responses to serotonin were significantly decreased in OVA cells compared to SAL cells grown on plastic, but this was not seen in cells grown on any other matrix. These experiments will help contribute to our understanding of ECM and its potential effects on mechanisms involved in smooth muscle contraction.
Les asthmatiques se caractérisent par un remodelage des voies respiratoires, incluant des changements dans la matrice extracellulaire et une augmentation de muscle lisse des voies respiratoires (MLVR). Aussi, les muscles lisses des asthmatiques ont une contractilité augmentée. Récemment on a montré qu'en changeant la matrice extracellulaire sur laquelle les muscles lisses sont cultivés, on peut affecter leur prolifération et l'apoptose. Mais on ne sait pas encore si la matrice extracellulaire peut affecter la contractilité des muscles lisses. Les muscles lisses ont été isolés des rats « Brown Norway » qui ont été sensibilisés avec l'ovalbumine (OVA) et ont été provoqués avec OVA ou saline (SAL) comme contrôle. Des cellules ont été semées sur un contrôle plastique ou sur des plats enduits de collagène (col), de décorine (dcn), ou de biglycane (bgn). Le niveau des protéines contractiles et la réponse du Ca2+ à l'ajout de serotonine dans une cellule unique a été mesuré. Les cellules OVA et SAL du MLVR qui ont été cultivées sur du col ont montré une réduction substantielle de leur contenu en α-SMA et calponine. Quand cultivées sur du bgn, une augmentation considérable du α-SMA et du calponine a été observée dans les cellules OVA du MLVR mais ceci n'a pas été observé sur des cellules SAL. Cependant quand on a semé les cellules SAL et OVA avec dcn, on n'a pas observé un effet significatif du niveau de calponine et α-SMA. La réaction du Ca2+ à la serotonine a diminué substantiellement dans les cellules OVA en comparaison à l'effet remarqué dans les cellules SAL, quand ces cellules ont été cultivées sur un contrôle plastique. Ces expériences contribuent à notre compréhension de l'importance des matrices extracellulaires dans leur contribution de l'augmentation de la contractilité du MLVR tel que décrit dans l'asthme.
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35

Hurst, Denise. "AMP-activated protein kinase kinase activity and phosphorylation of AMP-activated protein kinase in contracting muscle of sedentary and endurance trained rats." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd2014.pdf.

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36

Hawari, Omar. "Potential Role of αKAP, a CaMKII Kinase Anchoring Protein in Myocardium." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24299.

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The Sarco-endoplasmic Ca2+ ATPase (SERCA2a) plays a crucial role in sequestering cytosolic calcium into the sarco-endoplasmic reticulum (SR/ER) and is an important regulator of muscle contraction and relaxation. Recent findings suggest that a novel CAMKIIα splice variant, αKAP, that plays the role of a CAMKII anchoring protein in the myocardium, also directly interacts with SERCA2a. We examined the effects of αKAP on SERCA2a activity using transfection of HEK-293T cells as well as lentiviral infection of primary neonatal mouse cardiomyocytes (NMCM). Our data showed that αKAP reduced Ca2+ ATPase activity, and downregulated SERCA2a expression in both HEK-293T cells coexpressing αKAP and SERCA2a, as well as NMCM overexpressing αKAP. Interestingly in a rat model of myocardial infarction, αKAP expression was found to be elevated, alongside elevated CaMKIIδ, and depressed SERCA2a expression. These data suggest that αKAP may be a unique regulator of SERCA2a activity and cardiac function.
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37

Diering, Simon [Verfasser], and Friederike [Akademischer Betreuer] Cuello. "The impact of protein oxidation on kinase-mediated phosphorylation and cardiac myocyte contractile function / Simon Diering ; Betreuer: Friederike Cuello." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1182537863/34.

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38

Vannier, Catherine. "Modulation hormonale et pharmacologique de la sensibilite au calcium des proteines contractiles au cours de l'inotropisme cardiaque." Paris 11, 1996. http://www.theses.fr/1996PA112129.

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La force contractile du muscle cardiaque est determinee par les interactions actine myosine sous le controle des ions calcium. Cette force peut etre modulee par des mecanismes affectant la concentration intracellulaire en calcium ou la sensibilite au calcium des myofilaments. Grace a la mise en uvre de deux techniques experimentales, les variations sinusoidales de la longueur a differentes longueur de sarcomere et le bref raccourcissement/reetirement, la cinetique des ponts actine-myosine a ete etudiee sur des cellules de cur de rat isolees pelees au triton x-100. Dans les conditions controles, l'ion calcium est un element modulateur de la cinetique des ponts actine-myosine. En effet, k#t#r, la constante de temps de redeveloppement de la force apres un episode bref de raccourcissement/reetirement de la longueur de sarcomeres, augmente avec l'augmentation de la concentration en ions calcium. Malgre la presence d'isoformes specifiques des proteines contractiles regulatrices dans le muscle cardiaque et squelettique, une similitude des effets des ions calcium dans ces deux types de muscles est demontree dans ce travail contrairement a ce qui a ete generalement propose. En presence d'emd 57033, un sensibilisateur au calcium d'ordre pharmacologique, le temps d'attachement des ponts actine myosine est accrue. La reduction de l'energie consommee peut s'expliquer par une augmentation du temps passe par les ponts sous la forme generant de la force. De meme, apres stimulation #1-adrenergique, stimulation entrainant un effet inotrope positif avec augmentation de la sensibilite au calcium des proteines contractiles sans variation de la concentration en calcium intracellulaire, le temps d'attachement des ponts actine-myosine est augmente alors qu'il est reduit sur des cellules stimulees par un agoniste -adrenergique. Les ions seleniums sont responsables d'alterations de l'etat de reductions des ponts thiols, reduisent le courant ca et diminue la transitoire calcique. La force contractile est augmentee en presence ces ions, ce phenomene est attribue a une sensibilisation au calcium des proteines contractiles. Une modification des constantes de temps d'attachement et de detachement des ponts actine-myosine permet de rendre compte les variations pharmacologiques et hormonales de la contractilite myocardique
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39

Wretman, Charlott. "Changes in mitogen-activated protein kinase phosphorylation and inorganic phosphate induced by skeletal muscle contraction /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-320-1/.

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40

Goodall, Craig Ryan. "Determining Variations in the Expression and Activation-States of Key Cardiac Contraction Regulatory Proteins during HCM Disease Progression." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/320131.

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41

Stary, Creed Michael. "Contraction-induced elevation of heat shock protein 72 mRNA content in isolated single skeletal muscle fibers." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3211911.

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Thesis (Ph. D.)--University of California, San Diego, 2006.
Title from first page of PDF file (viewed Jul 10, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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42

SONG, QIUJING. "EFFECTS OF GENETIC MANIPULATION OF PHOSPHOLAMBAN PROTEIN LEVELS ON CONTRACTILE FUNCTION AND REMODELING IN MURINE CARDIAC AND SLOW-TWITCH SKELETAL MUSCLES." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1100807947.

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43

Ducommun, Bernard. "Regulation quantitative des tubulines au cours du cycle cellulaire chez le myxomycete physarum." Toulouse 3, 1988. http://www.theses.fr/1988TOU30131.

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Ng, Fung-kei, and 吳鋒奇. "The influence of a protein kinase A inhibitor on interstitial adenosine of muscle at rest and during contraction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45830708.

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45

Flinn, Rory J. "Novel use of glycosylation scanning to map the intracellular trafficking of sarco(endo)plasmic reticulum calcium ATPase 1A." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 0.55 Mb., 80 p, 2005. http://wwwlib.umi.com/dissertations/fullcit/1428192.

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46

Crockford, Tony. "The effects of temperature acclimation on the expression of contractile protein isoforms in the skeletal muscle of the common carp (Cyprinus carpio)." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/14940.

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Chapter 1. Part A reviews the current knowledge of temperature acclimation in teleost fish,with particular emphasis on skeletal muscle. There appear to be two types of response to low temperatures, dormancy or a homeostatic response. The homeostatic response serves to compensate for the reduced reaction rate usually seen at lower temperatures. In some species both responses occur depending on the water temperature. Part B reviews polymorphism in muscle proteins. All the myofibrillar proteins have been shown to exist as isoforms, which are differentially expressed in muscle types and with development. The isoforms expressed appear to be related to the contractile properties of the muscle. Chapter 2. The parvalbumin content, isoforms, and calcium binding characteristics were studied in the white muscle of 5° and 25° acclimated carp (Cyprinus carpio). The total parvalbumin concentration was 0.61-0.68mmols/kg wet weight. Two calcium binding sites per molecule and a dissociation constant of 2.1-2.4x10-6 M were measured. No differences related to acclimation temperature were observed. Chapter 3. The myofibrillar ATPase from white muscle of 8° and 20°C acclimated carp (Cyprinus carpio) u/as shown to increase in cold-acclimated fish at both high and low assay temperatures. Electrophoretic analysis of the myofibrillar proteins showed a unique myosin light chain isoform to be present in cold-acclimated fish, and a unique troponin I isoform to be present in warm acclimated fish. The presence of tropomyosin and troponin T isoforms in carp white muscle was also noted. The (MLC3 + extra MLC):MLC1 ratio was found to be lower in cold- than in warm-acclimated fish Chapter 4. Myosin heavy chains and actin from the white muscle of carp (Cyprinus carpio) acclimated to 2°, 5°, 8°, 11° C, 15°, and 23° were studied by peptide mapping. No differences were found between fish from any of the acclimation temperatures for either protein. Chapter 5. The major findings of the study are discussed, in relation to the mechanisms that produce protein isoforms, and with reference to further studies.
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47

Bichraoui, Hicham. "Identification de nouveaux déterminants moléculaires de l'interaction du récepteur des dihydropyridines avec le récepteur à la ryanodine." Université Joseph Fourier (Grenoble), 2010. https://tel.archives-ouvertes.fr/tel-00615499.

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L'excitation nerveuse d'une cellule musculaire produit une libération massive dans le cytoplasme du Ca2+ stocké dans le réticulum sarcoplasmique (RS). L'augmentation de la concentration cytoplasmique de Ca2+ déclenche la contraction. Ce processus, appelé couplage excitation contraction (CEC), requiert des interactions physiques entre deux canaux calciques: (1) le récepteur des dihydropyridines (DHPR), un canal calcique activé par le voltage ; le DHPR est composé de plusieurs sous-unités, dont la sous-unité α1S, qui forme le canal et le détecteur de potentiel, et la sous-unité ß1a, entièrement cytoplasmique; (2) le récepteur à la ryanodine (RyR1) responsable de la libération de Ca2+ hors du RS. La sous unité ß1a interagit avec la sous-unité α1S et RyR1. Au cours de ma thèse, j'ai identifié de nouveaux déterminants moléculaires et structuraux de l'interaction DHPR/RyR1. J'ai ainsi démontré l'existence d'interactions intramoléculaires entre les différentes boucles cytoplasmiques de la sous-unité α1S du DHPR, centrées autour d'un domaine appelé domaine A. J'ai également localisé le site d'interaction de la cavéoline-3 sur une boucle cytoplasmique de la sous-unité α1S. L'étude de l'interaction de la sous-unité ß1a avec RyR1 a montré (1) que la région C-terminale de ß1a contrôle cette interaction, (2) que l'affinité apparente de ß1a pour RyR1 est fortement augmentée par l'interaction de ß1a avec α1S et (3) que l'interaction ß1a/RyR1 régule la fermeture du RyR. L'utilisation d'une toxine, la maurocalcine (MCa) qui se comporte comme un analogue du domaine A m'a permis d'identifier un domaine minimal de RyR1 responsable de la fixation de la MCa et du domaine A. Une étude structurale par RMN de ce site a été réalisée. Enfin, j'ai étudié l'effet de la MCa sur des myotubes n'exprimant pas la sous-unité α1S. J'ai montré que la MCa est capable de restaurer, en absence de DHPR, une augmentation de la concentration de Ca2+ cytoplasmique induite par la dépolarisation de la membrane plasmique
In skeletal muscle, the action potential triggers muscle contraction through a massive calcium release from the sarcoplasmic reticulum (SR). This process, called excitation-contraction coupling (ECC), requires physical interactions between two calcium channels: (1) the dihydropyridine receptor (DHPR), a voltage-dependent channel composed of four subunits among which the α1S subunit, that forms both the pore and the voltage-sensor, and the ß1a subunit fully cytoplasmic, and (2) the ryanodine receptor (RyR1) which is responsible of calcium release from SR. ß1a subunit interacts with both RyRl and the α1S subunit. The mechanism whereby the DHPR is functionally coupled to RyR1 is still not clearly understood. During my thesis, I identified new molecular and structural determinants of the interaction between RyR and DHPR. I demonstrated the existence of intramolecular interactions between the cytoplasmic loops of the α1S subunit centered on a domain called domain A. I also localized the site of interaction of the caveoline-3 on the 1-11 loop of al S. The study of the interaction of the ßla subunit with RyR1 showed (1) that the C-terminal region of ß1a controls this interaction, (2) that the affinity of this interaction is strongly increased by the interaction of ß1a with α1S, and 3) that the interaction ß1a/RyR1 regulates the closure of RyR1. The use of a toxin, the maurocalcine (MCa) which behaves as an analogue of the domain A allowed me to identify a minimal domain of RyR1 responsible for the binding of the MCa and the domain A. A structural study by NMR of this domain has been realized. Finally, I studied the effect of the MCa on myotubes not expressing the α1S sub-unit. I showed that the MCa is capable of restoring in absence of DHPR, an increase of the cytoplasmic Ca2+ concentration triggered by the depolarization of the plasma membrane
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48

SCHMIT, BENNER ANNE-CATHERINE. "Le cytosquelette tubuline / f-actine de cellules de plantes superieures : identification, dynamique et interactions in vivo, en interphase et en mitose." Université Louis Pasteur (Strasbourg) (1971-2008), 1987. http://www.theses.fr/1987STR13123.

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49

Lidén, Åsa. "Integrin αVβ3-Directed Contraction by Connective Tissue Cells : Role in Control of Interstitial Fluid Pressure and Modulation by Bacterial Proteins." Doctoral thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6601.

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This thesis aimed at studying mechanisms involved in control of tissue fluid homeostasis during inflammation.

The interstitial fluid pressure (PIF) is of importance for control of tissue fluid balance. A lowering of PIF in vivo will result in a transport of fluid from the circulation into the tissue, leading to edema. Loose connective tissues that surround blood vessels have an intrinsic ability to take up fluid and swell. The connective tissue cells exert a tension on the fibrous network of the tissues, thereby preventing the tissues from swelling. Under normal homeostasis, the interactions between the cells and the fibrous network are mediated by β1 integrins. Connective tissue cells are in this way actively controlling PIF.

Here we show a previously unrecognized function for the integrin αVβ3, namely in the control of PIF. During inflammation the β1 integrin function is disturbed and the connective tissue cells release their tension on the fibrous network resulting in a lowering of PIF. Such a lowering can be restored by platelet-derived growth factor (PDGF) -BB. We demonstrated that PDGF-BB restored PIF through a mechanism that was dependent on integrin αVβ3. This was shown by the inability of PDGF-BB to restore a lowered PIF in the presence of anti-integrin β3 IgG or a peptide inhibitor of integrin αVβ3. PDGF-BB was in addition unable to normalize a lowered PIF in β3 null mice. Furthermore, we demonstrated that extracellular proteins from Streptococcus equi modulated αVβ3-mediated collagen gel contraction. Because of the established concordance between collagen gel contraction in vitro and control of PIF in vivo, a potential role for these proteins in control of tissue fluid homeostasis during inflammation could be assumed. Sepsis and septic shock are severe, and sometimes lethal, conditions. Knowledge of how bacterial components influence PIF and the mechanisms for tissue fluid control during inflammatory reactions is likely to be of clinical importance in treating sepsis and septic shock.

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50

Moreno-Gonzalez, Alicia. "Mechanical properties of myocardium following cardiomyocyte transplantation into infarcted hearts and investigations of the role of troponin C Ca2+ binding kinetics in skeletal muscle contraction /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8053.

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