Localization of Phospho-β-dystroglycan (pY892) to an Intracellular Vesicular Compartment in Cultured Cells and Skeletal Muscle Fibers in Vivo†

Biochemistry ◽  
2003 ◽  
Vol 42 (23) ◽  
pp. 7110-7123 ◽  
Author(s):  
Federica Sotgia ◽  
Gloria Bonuccelli ◽  
Mark Bedford ◽  
Andrea Brancaccio ◽  
Ulrike Mayer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cultured Cells ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers ◽  
Vesicular Compartment

scholarly journals Defective Acetylcholine Receptor Subunit Switch Precedes Atrophy of Slow-Twitch Skeletal Muscle Fibers Lacking ERK1/2 Kinases in Soleus Muscle

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuo Wang ◽  
Bonnie Seaberg ◽  
Ximena Paez-Colasante ◽  
Mendell Rimer
Keyword(s):  
Skeletal Muscle ◽  
Acetylcholine Receptor ◽  
Soleus Muscle ◽  
Muscle Fibers ◽  
Neuromuscular Synapse ◽  
Fiber Morphology ◽  
Skeletal Muscle Fibers ◽  
Slow Twitch

Abstract To test the role of extracellular-signal regulated kinases 1 and 2 (ERK1/2) in slow-twitch, type 1 skeletal muscle fibers, we studied the soleus muscle in mice genetically deficient for myofiber ERK1/2. Young adult mutant soleus was drastically wasted, with highly atrophied type 1 fibers, denervation at most synaptic sites, induction of “fetal” acetylcholine receptor gamma subunit (AChRγ), reduction of “adult” AChRε, and impaired mitochondrial biogenesis and function. In weanlings, fiber morphology and mitochondrial markers were mostly normal, yet AChRγ upregulation and AChRε downregulation were observed. Synaptic sites with fetal AChRs in weanling muscle were ~3% in control and ~40% in mutants, with most of the latter on type 1 fibers. These results suggest that: (1) ERK1/2 are critical for slow-twitch fiber growth; (2) a defective γ/ε-AChR subunit switch, preferentially at synapses on slow fibers, precedes wasting of mutant soleus; (3) denervation is likely to drive this wasting, and (4) the neuromuscular synapse is a primary subcellular target for muscle ERK1/2 function in vivo.

Ischemia/reperfusion-induced changes in intracellular free Ca2+ levels in rat skeletal muscle fibers – an in vivo study

2000 ◽  
Vol 440 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Tamás Ivanics ◽  
Zsuzsa Miklós ◽  
Zoltán Ruttner ◽  
Sándor Bátkai ◽  
Dick W. Slaaf ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
In Vivo Study ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Induced Changes

scholarly journals In Vivo Fatigue Reduces In Vitro Performance In Human Skeletal Muscle Fibers

2021 ◽  
Vol 53 (8S) ◽  
pp. 110-111
Author(s):  
Austin W. Ricci ◽  
Scott J. Mongold ◽  
Grace E. Privett ◽  
Karen W. Needham ◽  
Damien M. Callahan
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers ◽  
In Vitro Performance

scholarly journals Effects of dihydropyridine receptor II-III loop peptides on Ca2+ release in skinned skeletal muscle fibers

2000 ◽  
Vol 279 (4) ◽  
pp. C891-C905 ◽  
Author(s):  
Graham D. Lamb ◽  
Roque El-Hayek ◽  
Noriaki Ikemoto ◽  
D. George Stephenson
Keyword(s):  
Skeletal Muscle ◽  
Direct Action ◽  
Muscle Fibers ◽  
Dihydropyridine Receptor ◽  
Intracellular Loop ◽  
Release Channel ◽  
Voltage Sensors ◽  
Skeletal Muscle Fibers ◽  
Peptide Segments

In skeletal muscle fibers, the intracellular loop between domains II and III of the α1-subunit of the dihydropyridine receptor (DHPR) may directly activate the adjacent Ca2+ release channel in the sarcoplasmic reticulum. We examined the effects of synthetic peptide segments of this loop on Ca2+ release in mechanically skinned skeletal muscle fibers with functional excitation-contraction coupling. In rat fibers at physiological Mg2+ concentration ([Mg2+]; 1 mM), a 20-residue skeletal muscle DHPR peptide [AS(20); Thr671-Leu690; 30 μM], shown previously to induce Ca2+ release in a triad preparation, caused only small spontaneous force responses in ∼40% of fibers, although it potentiated responses to depolarization and caffeine in all fibers. The COOH-terminal half of AS(20)[AS(10)] induced much larger spontaneous responses but also caused substantial inhibition of Ca2+release to both depolarization and caffeine. Both peptides induced or potentiated Ca2+ release even when the voltage sensors were inactivated, indicating direct action on the Ca2+ release channels. The corresponding 20-residue cardiac DHPR peptide [AC(20); Thr793-Ala812] was ineffective, but its COOH-terminal half [AC(10)] had effects similar to AS(20). In the presence of lower [Mg2+] (0.2 mM), exposure to either AS(20) or AC(10) (30 μM) induced substantial Ca2+ release. Peptide CS (100 μM), a loop segment reported to inhibit Ca2+ release in triads, caused partial inhibition of depolarization-induced Ca2+ release. In toad fibers, each of the A peptides had effects similar to or greater than those in rat fibers. These findings suggest that the A and C regions of the skeletal DHPR II-III loop may have important roles in vivo.

scholarly journals Contraction and AICAR Stimulate IL-6 Vesicle Depletion From Skeletal Muscle Fibers In Vivo

Diabetes ◽  
2013 ◽  
Vol 62 (9) ◽  
pp. 3081-3092 ◽  
Author(s):  
Hans P.M.M. Lauritzen ◽  
Josef Brandauer ◽  
Peter Schjerling ◽  
Ho-Jin Koh ◽  
Jonas T. Treebak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers

scholarly journals Skeletal muscle fibers play a functional role in host defense during sepsis in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Orlando Laitano ◽  
Gerard P. Robinson ◽  
Kevin O. Murray ◽  
Christian K. Garcia ◽  
Alex J. Mattingly ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Inflammatory Responses ◽  
Muscle Fibers ◽  
Whole Body ◽  
Female Mice ◽  
Skeletal Muscle Fibers ◽  
Plasma Cytokines ◽  
Dependent Signal ◽  
Toll Receptor

AbstractSkeletal muscles secrete a wide variety of immunologically active cytokines, but the functional significance of this response to in vivo innate immunity is not understood. We addressed this by knocking out the toll receptor adapter protein, Myd88, only in skeletal muscle fibers (skmMyd88KO), and followed male and female mice at 6 and 12 h after peritoneal injection of cecal slurry (CS), a model of polymicrobial sepsis. Because of a previously identified increase in mortality to CS injection, males received ~ 30% lower dose. At 12 h, skmMyd88KO caused significant reductions in a wide variety of pro- and anti-inflammatory plasma cytokines, e.g. TNFα, IL-1β and IL-10, compared to strain-matched controls in both males and females. Similar reductions were observed at 6 h in females. SkmMyd88KO led to ~ 40–50% elevations in peritoneal neutrophils at 6 and 12 h post CS in females. At 12 h post CS, skmMyd88KO increased peritoneal monocytes/macrophages and decreased %eosinophils and %basophils in females. SkmMyd88KO also led to significantly higher rates of mortality in female mice but not in males. In conclusion, the results suggest that skeletal muscle Myd88-dependent signal transduction can play functionally important role in normal whole body, innate immune inflammatory responses to peritoneal sepsis.

The Collapse of the Sarcoplasmic Reticulum in Skeletal Muscle

1978 ◽  
Vol 33 (7-8) ◽  
pp. 561-573 ◽  
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace ◽  
Wilhelm Hasselbach
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Muscle Fibers ◽  
Membrane Capacitance ◽  
Frog Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Plausible Mechanism

Abstract When various cations, including Ca2+, are in the fixative, both sarcoplasmic reticulum (SR) of whole skeletal muscle and isolated SR vesicles collapse to form pentalaminate “compound membranes” that result from the apparent fusion of the lumenal lamellae of the membranous envelope of the SR. The process may be reversed by subsequently soaking the tissue in 1 ᴍ NaCl. An identical morphological phenomenon is observed in unfixed quickly frozen isolated frog skeletal muscle fibers, the cation in that case coming from endogenous sources. The hypothesis is advanced that the collapse is an in vivo process mediated by the sequestration of Ca2+ after contraction. The resulting obliteration of the SR lumen would have the effect of displacing the SR contents into the junctional SR, as well as electrically isolating the free SR from the junctional SR during relaxation. As a consequence, resistive coupling between the plasmalemma and the junctional SR becomes a plausible mechanism for the translation of the action potential into Ca2+ release, since the bulk of the SR membrane capacitance would now remain separated from the plasmalemma during relaxation.

scholarly journals Lymph flow pattern in pleural diaphragmatic lymphatics during intrinsic and extrinsic isotonic contraction

2016 ◽  
Vol 310 (1) ◽  
pp. H60-H70 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Skeletal Muscle ◽  
Shear Stress ◽  
Muscle Contraction ◽  
Ex Vivo ◽  
Muscle Fibers ◽  
Lymphatic Vessels ◽  
Smooth Muscle Contraction ◽  
Skeletal Muscle Fibers ◽  
Skeletal Muscle Contraction

Peripheral rat diaphragmatic lymphatic vessels, endowed with intrinsic spontaneous contractility, were in vivo filled with fluorescent dextrans and microspheres and subsequently studied ex vivo in excised diaphragmatic samples. Changes in diameter and lymph velocity were detected, in a vessel segment, during spontaneous lymphatic smooth muscle contraction and upon activation, through electrical whole-field stimulation, of diaphragmatic skeletal muscle fibers. During intrinsic contraction lymph flowed both forward and backward, with a net forward propulsion of 14.1 ± 2.9 μm at an average net forward speed of 18.0 ± 3.6 μm/s. Each skeletal muscle contraction sustained a net forward-lymph displacement of 441.9 ± 159.2 μm at an average velocity of 339.9 ± 122.7 μm/s, values significantly higher than those documented during spontaneous contraction. The flow velocity profile was parabolic during both spontaneous and skeletal muscle contraction, and the shear stress calculated at the vessel wall at the highest instantaneous velocity never exceeded 0.25 dyne/cm2. Therefore, we propose that the synchronous contraction of diaphragmatic skeletal muscle fibers recruited at every inspiratory act dramatically enhances diaphragmatic lymph propulsion, whereas the spontaneous lymphatic contractility might, at least in the diaphragm, be essential in organizing the pattern of flow redistribution within the diaphragmatic lymphatic circuit. Moreover, the very low shear stress values observed in diaphragmatic lymphatics suggest that, in contrast with other contractile lymphatic networks, a likely interplay between intrinsic and extrinsic mechanisms be based on a mechanical and/or electrical connection rather than on nitric oxide release.

Abstract 362: Deletion of Gata4 and Gata6 in the c-Kit Lineage Augments Cellular Fusion in vivo

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Bryan D Maliken ◽  
Onur Kanisicak ◽  
Jeffery D Molkentin
Keyword(s):  
Skeletal Muscle ◽  
Bone Marrow ◽  
Immune Cell ◽  
Muscle Fibers ◽  
Cell Activity ◽  
Fold Increase ◽  
Lineage Tracing ◽  
Skeletal Muscle Fibers ◽  
Cellular Fusion

Cell therapy for treatment of ischemic heart disease has been under rigorous evaluation in recent years. Heart-derived c-Kit cells showed promising results in clinical trials with scar reduction and improved ejection fraction following coronary infusion. We previously developed a c-Kit lineage tracing model showing that these cells very rarely convert into de novo cardiomyocytes. To potentially reduce this rate to zero, and unequivocally evaluate cellular fusion processes in vivo, we deleted the cardiogenic transcription factors Gata4 and Gata6 in c-Kit cells using a Cre-loxP approach (Kit-Gata4/6 KO). We used the tamoxifen inducible Kit-MerCreMer allele crossed into Gata4/6 homozygous LoxP targeted background and the Rosa26-eGFP reporter, which were given tamoxifen at weaning to delete Gata4 and Gata6 in all c-Kit expressing cells and show them and their progeny as eGFP positive. Unexpectedly, we observed a greater than 10-fold increase in Kit lineage-traced cardiomyocytes in some Kit-Gata4/6 KO mice compared to Kit only controls with up to 4 months of treatment. Exploration of other tissues revealed a dramatic increase in presumed Kit-lineage traced skeletal muscle fibers in Kit-Gata4/6 KO mice as well. However, investigation of this effect suggested that this increase in presumed Kit-lineage traced cardiomyocytes and skeletal muscle fibers was due to an alteration in the immune cell compartment of these mice that generated greater rates of fusion. Indeed, analysis of Kit-derived hematopoietic lineages present in the heart showed a 6-fold increase in leukocyte infiltration (CD45 + ) and a 60-fold increase in dendritic cells (CD11c + ) from Kit-Gata4/6 KO mice. Kit-eGFP + bone marrow was also transplanted into mice expressing a membrane tomato reporter. Kit-Gata4/6 KO bone marrow showed a 3-fold increase in Kit-eGFP cells, although all these myocytes had the membrane tomato tag indicting that these events were all due to fusion. Hence, alterations in c-Kit cell activity likely impacts the activity of the immune system and the fusigenic activity of derived cells.

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