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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
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Networked Digital Library of Theses and Dissertations.
Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
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Impairment of Diastolic Function by Lack of Frequency-Dependent Myofilament Desensitization in Rabbit Right Ventricular HypertrophyVarian, Kenneth D., Kijtawornrat, Anusak, Gupta, Subash C., Torres, Carlos A., Monasky, Michelle M., Hiranandani, Nitisha, Delfin, Dawn A., Rafael-Fortney, Jill A., Periasamy, Muthu, Hamlin, Robert L., Janssen, Paul M.L. 01 September 2009 (has links)
Background-Ventricular hypertrophy is a physiological response to pressure overload that, if left untreated, can ultimately result in ventricular dysfunction, including diastolic dysfunction. The aim of this study was to test the hypothesis that frequency-dependent myofilament desensitization, a physiological response of healthy myocardium, is altered in hypertrophied myocardium. Methods and Results-New Zealand white rabbits underwent a pulmonary artery banding procedure to induce pressure overload. After 10 weeks, the animals were euthanized, hearts removed, and suitable trabeculae harvested from the free wall of the right ventricle. Twitch contractions, calibrated bis-fura-2 calcium transients, and myofilament calcium sensitivity (potassium contractures) were measured at frequencies of 1, 2, 3, and 4 Hz. The force frequency response, relaxation frequency response, and calcium frequency relationships were significantly blunted, and diastolic tension significantly increased with frequency in the pulmonary artery banding rabbits compared with sham-operated animals. Myofilament calcium sensitivity was virtually identical at 1 Hz in the treatment versus sham group (pCa 6.11 ± 0.03 versus 6.11 ± 0.06), but the frequency-dependent desensitization that takes place in the sham group (ΔpCa 0.14±0.06, P<0.05) was not observed in the pulmonary artery banding animals (ΔpCa 0.02±0.05). Analysis of myofilament protein phosphorylation revealed that the normally observed frequency-dependent phosphorylation of troponin-I is lost in pulmonary artery banding rabbits. Conclusions-The frequency-dependent myofilament desensitization is significantly impaired in right ventricular hypertrophy and contributes to the frequency-dependent elevation of diastolic tension in hypertrophy.
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Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and ContractionCong, Xiaofei 01 February 2016 (has links)
The SH3 and cysteine rich domain 3 (Stac3) gene is expressed specifically in skeletal muscle and essential for skeletal muscle contraction and postnatal life in mice. In this dissertation project, I conducted two studies to further understand the role of STAC3 in skeletal muscle development, growth, and contraction. In the first study, I compared the contractile responses of hindlimb muscles of Stac3 knockout and control mice to electrical stimulation, high [K+]-induced membrane depolarization, and caffeine and 4-chloro-m-cresol (4-CMC) activation of ryanodine receptor (RyR). Frequent electrostimulation-, high [K+]-, 4-CMC- and caffeine-induced maximal tensions in Stac3-deleted muscles were approximately 20%, 29%, 58% and 55% of those in control muscles, respectively. 4-CMC- and caffeine-induced increases in intracellular calcium were not different between Stac3-deleted and control myotubes. Myosin-ATPase and NADH-tetrazolium reductase staining as well as gene expression analyses revealed that Stac3-deleted hindlimb muscles contained more slow type-like fibers than control muscles. These data together confirm a role of STAC3 in EC coupling but also suggest that defective EC coupling is only partially responsible for the significantly reduced contractility in Stac3-deleted hindlimb muscles. In the second study, I determined the potential role of STAC3 in postnatal skeletal muscle growth, fiber composition, and contraction by disrupting Stac3 gene expression in postnatal mice through the Flp-FRT and tamoxifen-inducible Cre-loxP systems. Postnatal Stac3 deletion inhibited body and limb muscle mass gains. Histological staining and gene expression analyses revealed that postnatal Stac3 deletion decreased the size of myofibers and increased the percentage of myofibers containing centralized nuclei without affecting the total myofiber number. Postnatal Stac3 deletion decreased limb muscle strength. Postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced maximal force output in limb muscles. Similarly, postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced calcium release from the sarcoplasmic reticulum. These results demonstrate that STAC3 is important to myofiber hypertrophy, myofiber type composition, contraction, and EC coupling in postnatal skeletal muscle. / Ph. D.
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Die Bedeutung der Kalzium/Calmodulin-abhängigen Proteinkinase II für den gestörten Kalziumstoffwechsel der isolierten Rattenherzmuskelzelle unter Doxorubicinbehandlung / Ca2+/Calmodulin-dependent protein kinase II contributes to impaired Ca2+ handling properties in isolated rat cardiomyocytes under doxorubicin treatmentKöhler, Anne Christine 08 July 2013 (has links)
No description available.
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Role of SLMAP in Endoplasmic Reticulum Stress and Unfolded Protein ResponseMahmood, Ahsan 13 August 2013 (has links)
Cardiac function is regulated by the molecular components of the sarco/endoplasmic reticulum (ER/SR). Disruptions in homeostatic balance of these proteins and calcium regulation results in activation of ER stress response. Sarcolemmal membrane-associated proteins (SLMAPs) are found in cell membrane, SR/ER, and mitochondria. Overexpression of SLMAP in the myocardium has shown to impair excitation-contraction (E-C) coupling in the transgenic (Tg) mice. ER stress response was examined in Tg mice overexpressing SLMAP in the myocardium. In Tg hearts, changes observed in the expression of proteins involved in ER stress were dependent on the age and sex. SLMAP overexpression results in maladaptive ER stress response, as the mice age. Neonatal cardiomyocytes isolated from the Tg hearts showed decreased viability, upregulation of ER stress response proteins, which were sensitized to thapsigargin-induced stress, and desensitized to palmitate-induced oxidative stress. These findings suggest that normal SLMAP levels are important for proper cardiac function, and cell viability.
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Role of SLMAP in Endoplasmic Reticulum Stress and Unfolded Protein ResponseMahmood, Ahsan January 2013 (has links)
Cardiac function is regulated by the molecular components of the sarco/endoplasmic reticulum (ER/SR). Disruptions in homeostatic balance of these proteins and calcium regulation results in activation of ER stress response. Sarcolemmal membrane-associated proteins (SLMAPs) are found in cell membrane, SR/ER, and mitochondria. Overexpression of SLMAP in the myocardium has shown to impair excitation-contraction (E-C) coupling in the transgenic (Tg) mice. ER stress response was examined in Tg mice overexpressing SLMAP in the myocardium. In Tg hearts, changes observed in the expression of proteins involved in ER stress were dependent on the age and sex. SLMAP overexpression results in maladaptive ER stress response, as the mice age. Neonatal cardiomyocytes isolated from the Tg hearts showed decreased viability, upregulation of ER stress response proteins, which were sensitized to thapsigargin-induced stress, and desensitized to palmitate-induced oxidative stress. These findings suggest that normal SLMAP levels are important for proper cardiac function, and cell viability.
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Auswirkungen des neuartigen CaMKII-Inhibitors SMP-114 auf das diastolische SR Ca2+-Leck und die elektromechanische Kopplung isolierter Herzmuskelzellen / Effects of the novel CaMKII inhibitor SMP-114 on diastolic SR Ca2+ leak and EC coupling in isolated cardiomyocitesMann, Christian 28 October 2015 (has links)
No description available.
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A Quantitative Manganese-Enhanced MRI Method For In Vivo Assessment Of L-Type Calcium Channel Activity In HeartLi, Wen 15 April 2011 (has links)
No description available.
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Altered Skeletal Muscle Excitation-Contraction Coupling in the R6/2 Transgenic Mouse Model for Huntington's DiseaseMiranda, Daniel R. January 2021 (has links)
No description available.
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