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  • 1
    Electronic Resource
    Electronic Resource
    Growth-related alterations in motor endplates of type-identified diaphragm muscle fibres (1995)
    Springer
    Journal of neurocytology 24 (1995), S. 225-235 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using a double-labelling technique, and dual-channel confocal microscopy, we examined the three-dimensional and two-dimensional morphologies of motor endplates on type I and II muscle fibres of 21-day-old and adult rat diaphragms. Motor endplates were visualized with fluorescein-conjugated α-bungarotoxin, and muscle fibre type was immunocytochemically determined using an anti-fast (type II) myosin antibody with a Cy5-conjugated label. Surface (three-dimensional) and planar (two-dimensional) areas were obtained from three-dimensional reconstructions of confocal optical sections of labelled endplates. Muscle fibre diameters were also measured. Total branch lengths were measured from projection images of the three dimensional reconstructions. The surface and planar areas of endplates on type I fibres at day 21 were larger than those on type II fibres, and this difference increased with maturation. In adults, the surface area of endplates was positively correlated to muscle fibre size, but such a correlation was not found at day 21. When normalized for fibre diameter, the surface areas of endplates on type I fibres were still significantly larger than those on type II fibres in both age groups. The normalized endplate surface area for type II fibres remained constant with maturation, whereas for type I fibres, the increase in endplate surface area was disproportionate to fibre growth.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01181536
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Morphology of diaphragm neuromuscular junctions on different fibre types (1996)
    Springer
    Journal of neurocytology 25 (1996), S. 88-100 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We hypothesize that the morphology of the neuromuscular junction on different muscle fibre types varies, reflecting differences in activation history. In the rat diaphragm muscle, we used a three-colour fluorescent immunocytochemical technique to simultaneously visualize (1) innervating axons and presynaptic nerve terminals, (2) motor endplates and (3) myosin heavy chain isoform expression (muscle fibre type). Laser-scanning confocal microscopy was then used to optically section the triple-labelled muscle fibres, and create three-dimensional views of the neuromuscular junction. Type I fibres were innervated by the smallest axons, and type IIa, IIx and IIb fibres by progressively larger axons. Absolute planar areas of nerve terminals and endplates progressively increased from type I, IIa, IIx to IIb fibres. When normalized for fibre diameter planar areas of nerve terminals were largest on type I fibres, with no difference among type II fibres. The normalized planar area of endplates were larger for type I and IIb fibres, compared to type IIa and IIx fibres. The three-dimensional surface area of endplates was largest on type I fibres, with no differences across type II fibres. When normalized for fibre diameter, endplate surface areas increase progressively from type I, IIa, IIx to IIb fibres. The branches increased progressively from type I, IIa, IIx to IIb fibres. Conversely, individual branch length was longest on type I fibres, and shortest on type IIb fibres. The extent of overlap of pre- and postsynaptic elements of the neuromuscular junction decreased progressively on type I, IIa, IIx and IIb fibres. We conclude that these morphological differences at the neuromuscular function of different fibre types reflect differences in activation history and may underlie phenotypic differences in neuromuscular transmission.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02284788
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  • 3
    Electronic Resource
    Electronic Resource
    Comparison of cross-bridge cycling kinetics in neonatal vs. adult rat ventricular muscle (1999)
    Springer
    Journal of muscle research and cell motility 20 (1999), S. 717-723 
    Details
    ISSN: 1573-2657
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The developmental shift in contractile protein isoform expression in the rodent heart likely affects actin-myosin cross-bridge interactions. We compared the Ca2+ sensitivity for force generation and cross-bridge cycling kinetics in neonatal (postnatal days 0–3) and adult (day 84) rats. The force-pCa relationship was determined in Triton-X skinned muscle bundles activated at pCa 9.0 to 4.0. In strips maximally activated at pCa 4.0, the following parameters of cross-bridge cycling were measured: (1) rate of force redevelopment following rapid shortening and restretching (ktr); and (2) isometric stiffness at maximal activation and in rigor. The fraction of attached cross-bridges (αfs) and apparent rate constants for cross-bridge attachment (fapp) and detachment (gapp) were derived assuming a two-state model for cross-bridge cycling. Compared to the adult, the force-pCa curve for neonatal cardiac muscle was significantly shifted to the left. Neonatal cardiac muscle also displayed significantly smaller αfs, slower ktr and fapp; however, gapp was not significantly different between age groups. These data indicate that weaker force production in neonatal cardiac muscle involves, at least in part, less efficient cross-bridge cycling kinetics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005585807179
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  • 4
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    TNF{alpha} decreases mitochondrial movement in human airway smooth muscle (2017)
    The American Physiological Society (APS)
    Details
    Publication Date: 2017-07-02
    Description: In airway smooth muscle (ASM) cells, excitation-contraction coupling is accomplished via a cascade of events that connect an elevation of cytosolic Ca 2+ concentration ([Ca 2+ ] cyt ) with cross-bridge attachment and ATP-consuming mechanical work. Excitation-energy coupling is mediated by linkage of the elevation of [Ca 2+ ] cyt to an increase in mitochondrial Ca 2+ concentration, which in turn stimulates ATP production. Proximity of mitochondria to the sarcoplasmic reticulum (SR) and plasma membrane is thought to be an important mechanism to facilitate mitochondrial Ca 2+ uptake. In this regard, mitochondrial movement in ASM cells may be key in establishing proximity. Mitochondria also move where ATP or Ca 2+ buffering is needed. Mitochondrial movement is mediated through interactions with the Miro-Milton molecular complex, which couples mitochondria to kinesin motors at microtubules. We examined mitochondrial movement in human ASM cells and hypothesized that, at basal [Ca 2+ ] cyt levels, mitochondrial movement is necessary to establish proximity of mitochondria to the SR and that, during the transient increase in [Ca 2+ ] cyt induced by agonist stimulation, mitochondrial movement is reduced, thereby promoting transient mitochondrial Ca 2+ uptake. We further hypothesized that airway inflammation disrupts basal mitochondrial movement via a reduction in Miro and Milton expression, thereby disrupting the ability of mitochondria to establish proximity to the SR and, thus, reducing transient mitochondrial Ca 2+ uptake during agonist activation. The reduced proximity of mitochondria to the SR may affect establishment of transient "hot spots" of higher [Ca 2+ ] cyt at the sites of SR Ca 2+ release that are necessary for mitochondrial Ca 2+ uptake via the mitochondrial Ca 2+ uniporter.
    Print ISSN: 1040-0605
    Electronic ISSN: 1522-1504
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 5
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    Novel Roles of Mitochondrial Uniporter in Ovarian Cancer [Cell Biology] (2013)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publication Date: 2013-06-15
    Description: Nanoparticles provide a potent tool for targeting and understanding disease mechanisms. In this regard, cancer cells are surprisingly resistant to the expected toxic effects of positively charged gold nanoparticles (+AuNPs). Our investigations led to the identification of MICU1, regulator of mitochondrial calcium uniporter, as a key molecule conferring cancer cells with resistance to +AuNPs. The increase in cytosolic [Ca2+]cyto in malignant cells induced by +AuNPs is counteracted by MICU1, preventing cell death. Pharmacological or siRNA-mediated inhibition of mitochondrial Ca+2 entry leads to endoplasmic reticulum stress and sensitizes cancer cells to +AuNP-induced cytotoxicity. Silencing MICU1 decreases Bcl-2 expression and increases caspase-3 activity and cytosolic cytochrome c levels, thus initiating the mitochondrial pathway for apoptosis: effects further enhanced by +AuNPs. This study highlights the potential of nanomaterials as a tool to broaden our understanding of cellular processes, establishes MICU1 as a novel regulator of the machinery in cancer cells that prevents apoptosis, and emphasizes the need to synergize nanoparticle design with understanding of mitochondrial machinery for enhancing targeted cellular toxicity.
    Print ISSN: 0021-9258
    Electronic ISSN: 1083-351X
    Topics: Biology , Chemistry and Pharmacology
    Published by The American Society for Biochemistry and Molecular Biology (ASBMB)
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  • 6
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    Inflammation alters regional mitochondrial Ca2+ in human airway smooth muscle cells (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-08-02
    Description: Regulation of cytosolic Ca 2+ concentration ([Ca 2+ ] cyt ) in airway smooth muscle (ASM) is a key aspect of airway contractility and can be modulated by inflammation. Mitochondria have tremendous potential for buffering [Ca 2+ ] cyt , helping prevent Ca 2+ overload, and modulating other intracellular events. Here, compartmentalization of mitochondria to different cellular regions may subserve different roles. In the present study, we examined the role of Ca 2+ buffering by mitochondria and mitochondrial Ca 2+ transport mechanisms in the regulation of [Ca 2+ ] cyt in enzymatically dissociated human ASM cells upon exposure to the proinflammatory cytokines TNF-α and IL-13. Cells were loaded simultaneously with fluo-3 AM and rhod-2 AM, and [Ca 2+ ] cyt and mitochondrial Ca 2+ concentration ([Ca 2+ ] mito ) were measured, respectively, using real-time two-color fluorescence microscopy in both the perinuclear and distal, perimembranous regions of cells. Histamine induced a rapid increase in both [Ca 2+ ] cyt and [Ca 2+ ] mito , with a significant delay in the mitochondrial response. Inhibition of the mitochondrial Na + /Ca 2+ exchanger (1 μM CGP-37157) increased [Ca 2+ ] mito responses in perinuclear mitochondria but not distal mitochondria. Inhibition of the mitochondrial uniporter (1 μM Ru360) decreased [Ca 2+ ] mito responses in perinuclear and distal mitochondria. CGP-37157 and Ru360 significantly enhanced histamine-induced [Ca 2+ ] cyt . TNF-α and IL-13 both increased [Ca 2+ ] cyt , which was associated with decreased [Ca 2+ ] mito in the case of TNF-α but not IL-13. The effects of TNF-α on both [Ca 2+ ] cyt and [Ca 2+ ] mito were affected by CGP-37157 but not by Ru360. Overall, these data demonstrate that in human ASM cells, mitochondria buffer [Ca 2+ ] cyt after agonist stimulation and its enhancement by inflammation. The differential regulation of [Ca 2+ ] mito in different parts of ASM cells may serve to locally regulate Ca 2+ fluxes from intracellular sources versus the plasma membrane as well as respond to differential energy demands at these sites. We propose that such differential mitochondrial regulation, and its disruption, may play a role in airway hyperreactivity in diseases such as asthma, where [Ca 2+ ] cyt is increased.
    Print ISSN: 0363-6143
    Electronic ISSN: 1522-1563
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 7
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    Estrogen effects on human airway smooth muscle involve cAMP and protein kinase A (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-11-16
    Description: Clinically observed differences in airway reactivity and asthma exacerbations in women at different life stages suggest a role for sex steroids in modulating airway function although their targets and mechanisms of action are still being explored. We have previously shown that clinically relevant concentrations of exogenous estrogen acutely decrease intracellular calcium ([Ca 2+ ] i ) in human airway smooth muscle (ASM), thereby facilitating bronchodilation. In this study, we hypothesized that estrogens modulate cyclic nucleotide regulation, resulting in decreased [Ca 2+ ] i in human ASM. In Fura-2-loaded human ASM cells, 1 nM 17β-estradiol (E 2 ) potentiated the inhibitory effect of the β-adrenoceptor (β-AR) agonist isoproterenol (ISO; 100 nM) on histamine-mediated Ca 2+ entry. Inhibition of protein kinase A (PKA) activity (KT5720; 100 nM) attenuated E 2 effects on [Ca 2+ ] i . Acute treatment with E 2 increased cAMP levels in ASM cells comparable to that of ISO (100 pM). In acetylcholine-contracted airways from female guinea pigs or female humans, E 2 potentiated ISO-induced relaxation. These novel data suggest that, in human ASM, physiologically relevant concentrations of estrogens act via estrogen receptors (ERs) and the cAMP pathway to nongenomically reduce [Ca 2+ ] i , thus promoting bronchodilation. Activation of ERs may be a novel adjunct therapeutic avenue in reactive airway diseases in combination with established cAMP-activating therapies such as β 2 -agonists.
    Print ISSN: 1040-0605
    Electronic ISSN: 1522-1504
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 8
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    Brain-derived neurotrophic factor and airway fibrosis in asthma (2017)
    The American Physiological Society (APS)
    Details
    Publication Date: 2017-08-04
    Description: Airway remodeling in asthma driven by inflammation involves proliferation of epithelial cells and airway smooth muscle (ASM), as well as enhanced extracellular matrix (ECM) generation and deposition, i.e., fibrosis. Accordingly, understanding profibrotic mechanisms is important for developing novel therapeutic strategies in asthma. Recent studies, including our own, have suggested a role for locally produced growth factors such as brain-derived neurotrophic factor (BDNF) in mediating and modulating inflammation effects. In this study, we explored the profibrotic influence of BDNF in the context of asthma by examining expression, activity, and deposition of ECM proteins in primary ASM cells isolated from asthmatic vs. nonasthmatic patients. Basal BDNF expression and secretion, and levels of the high-affinity BDNF receptor TrkB, were higher in asthmatic ASM. Exogenous BDNF significantly increased ECM production and deposition, especially of collagen-1 and collagen-3 (less so fibronectin) and the activity of matrix metalloproteinases (MMP-2, MMP-9). Exposure to the proinflammatory cytokine TNFα significantly increased BDNF secretion, particularly in asthmatic ASM, whereas no significant changes were observed with IL-13. Chelation of BDNF using TrkB-Fc reversed TNFα-induced increase in ECM deposition. Conditioned media from asthmatic ASM enhanced ECM generation in nonasthmatic ASM, which was blunted by BDNF chelation. Inflammation-induced changes in MMP-2, MMP-9, and tissue inhibitor metalloproteinases (TIMP-1, TIMP-2) were reversed in the presence of TrkB-Fc. These novel data suggest ASM as an inflammation-sensitive source of BDNF within human airways, with autocrine effects on fibrosis relevant to asthma.
    Print ISSN: 1040-0605
    Electronic ISSN: 1522-1504
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 9
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    Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease (2016)
    The American Physiological Society (APS)
    Details
    Publication Date: 2016-12-14
    Description: Airway structure and function are key aspects of normal lung development, growth, and aging, as well as of lung responses to the environment and the pathophysiology of important diseases such as asthma, chronic obstructive pulmonary disease, and fibrosis. In this regard, the contributions of airway smooth muscle (ASM) are both functional, in the context of airway contractility and relaxation, as well as synthetic, involving production and modulation of extracellular components, modulation of the local immune environment, cellular contribution to airway structure, and, finally, interactions with other airway cell types such as epithelium, fibroblasts, and nerves. These ASM contributions are now found to be critical in airway hyperresponsiveness and remodeling that occur in lung diseases. This review emphasizes established and recent discoveries that underline the central role of ASM and sets the stage for future research toward understanding how ASM plays a central role by being both upstream and downstream in the many interactive processes that determine airway structure and function in health and disease.
    Print ISSN: 1040-0605
    Electronic ISSN: 1522-1504
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 10
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    NHERF-2 maintains endothelial homeostasis (2012)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2012-05-18
    Description: The Na + /H + exchanger regulatory factor-2 (NHERF-2) is an integral component of almost all endothelial cells (ECs), yet its endothelial function is not known. Here, we found that NHERF-2, is a key regulator of endothelial homeostasis because NHERF-2–silenced ECs proliferate at a much higher rate even in the absence of mitogens such as VEGF compared with control ECs. We further show that the hyperproliferation phenotype of NHERF-2–silenced EC is because of an accelerated cell cycle that is probably caused by a combination of the following factors: increased cytoplasmic calcium, increased expression of c-Myc, increased expression of cyclin D1, and reduced expression of p27. Using an experimental mouse model of human hemangioma, we found that the endothelial neoplasms derived from NHERF-2–silenced cells were much larger in volume than those derived from control cells. Thus, NHERF-2 is a negative regulator of endothelial proliferation and may have important roles in endothelial homeostasis and vascular modeling.
    Keywords: Vascular Biology
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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