THE APPARENT EXTRACELLULAR SPACE OF MAMMALIAN SKELETAL MUSCLE: A COMPARISON OF THE INULIN SPACE IN NORMAL AND DYSTROPHIC MOUSE TISSUES

1960 ◽  
Vol 38 (8) ◽  
pp. 829-835 ◽  
Author(s):  
L. H. Burr ◽  
H. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Normal Tissue ◽  
Muscle Size ◽  
Mammalian Skeletal Muscle ◽  
Normal Tissues ◽  
Mouse Tissues ◽  
Inulin Space ◽  
Excised Tissues ◽  
Dystrophic Mice

The apparent extracellular volumes of the muscles from young normal and dystrophic mice have been estimated, using inulin dilution techniques. The inulin spaces were measured in the muscle both following injection of inulin in vivo and after soaking of excised tissues in a solution containing inulin. Comparisons were made between muscles of different size from the same animal as well as from different animals whose age, and consequently muscle size, varied. In all cases it has been found that the inulin space decreases with increasing muscle size. Similar results have been obtained by others with toad sartorii. The inulin space in muscles from dystrophic mice is larger than that of comparable normal tissues, and the dependence on muscle size, although similar to normal, is more pronounced. The results suggest that the dystrophic cells are permeable to inulin, and the question that some small permeability may be present also in normal tissue is considered.

THE APPARENT EXTRACELLULAR SPACE OF MAMMALIAN SKELETAL MUSCLE: A COMPARISON OF THE INULIN SPACE IN NORMAL AND DYSTROPHIC MOUSE TISSUES

1960 ◽  
Vol 38 (1) ◽  
pp. 829-835 ◽  
Author(s):  
L. H. Burr ◽  
H. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Normal Tissue ◽  
Muscle Size ◽  
Mammalian Skeletal Muscle ◽  
Normal Tissues ◽  
Mouse Tissues ◽  
Inulin Space ◽  
Excised Tissues ◽  
Dystrophic Mice

The apparent extracellular volumes of the muscles from young normal and dystrophic mice have been estimated, using inulin dilution techniques. The inulin spaces were measured in the muscle both following injection of inulin in vivo and after soaking of excised tissues in a solution containing inulin. Comparisons were made between muscles of different size from the same animal as well as from different animals whose age, and consequently muscle size, varied. In all cases it has been found that the inulin space decreases with increasing muscle size. Similar results have been obtained by others with toad sartorii. The inulin space in muscles from dystrophic mice is larger than that of comparable normal tissues, and the dependence on muscle size, although similar to normal, is more pronounced. The results suggest that the dystrophic cells are permeable to inulin, and the question that some small permeability may be present also in normal tissue is considered.

In vivo supraspinatus muscle contractility and architecture in rabbit

2020 ◽  
Vol 129 (6) ◽  
pp. 1405-1412
Author(s):  
Sydnee A. Hyman ◽  
Mackenzie B. Norman ◽  
Shanelle N. Dorn ◽  
Shannon N. Bremner ◽  
Mary C. Esparza ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Isometric Force ◽  
Muscle Physiology ◽  
Mammalian Skeletal Muscle ◽  
Improved Method ◽  
Muscle Contractility ◽  
Supraspinatus Muscle ◽  
Contractile Stress ◽  
Maximum Isometric Force

We introduce an improved method to assess rabbit supraspinatus muscle physiology. Maximum isometric force measured for the rabbit supraspinatus was dramatically greater than previous reports in the literature. Consequently, the isometric contractile stress reported is almost 10 times greater than previous reports of rabbit supraspinatus, but similar to available literature of other mammalian skeletal muscle. We show that previous reports of peak supraspinatus isometric force were subphysiological by ∼90%

scholarly journals Dynamics of Myoblast Transplantation Reveal a Discrete Minority of Precursors with Stem Cell–like Properties as the Myogenic Source

1999 ◽  
Vol 144 (6) ◽  
pp. 1113-1122 ◽  
Author(s):  
Jonathan R. Beauchamp ◽  
Jennifer E. Morgan ◽  
Charles N. Pagel ◽  
Terence A. Partridge
Keyword(s):  
Cell Cycle ◽  
Skeletal Muscle ◽  
Tissue Culture ◽  
Stem Cell ◽  
Genetic Modification ◽  
Muscle Formation ◽  
Myoblast Transplantation ◽  
Dystrophic Mice

Myoblasts, the precursors of skeletal muscle fibers, can be induced to withdraw from the cell cycle and differentiate in vitro. Recent studies have also identified undifferentiated subpopulations that can self-renew and generate myogenic cells (Baroffio, A., M. Hamann, L. Bernheim, M.-L. Bochaton-Pillat, G. Gabbiani, and C.R. Bader. 1996. Differentiation. 60:47–57; Yoshida, N., S. Yoshida, K. Koishi, K. Masuda, and Y. Nabeshima. 1998. J. Cell Sci. 111:769–779). Cultured myoblasts can also differentiate and contribute to repair and new muscle formation in vivo, a capacity exploited in attempts to develop myoblast transplantation (MT) for genetic modification of adult muscle. Our studies of the dynamics of MT demonstrate that cultures of myoblasts contain distinct subpopulations defined by their behavior in vitro and divergent responses to grafting. By comparing a genomic and a semiconserved marker, we have followed the fate of myoblasts transplanted into muscles of dystrophic mice, finding that the majority of the grafted cells quickly die and only a minority are responsible for new muscle formation. This minority is behaviorally distinct, slowly dividing in tissue culture, but rapidly proliferative after grafting, suggesting a subpopulation with stem cell–like characteristics.

scholarly journals Muscle-Derived Extracellular Signal-Regulated Kinases 1 and 2 Are Required for the Maintenance of Adult Myofibers and Their Neuromuscular Junctions

2015 ◽  
Vol 35 (7) ◽  
pp. 1238-1253 ◽  
Author(s):  
Bonnie Seaberg ◽  
Gabrielle Henslee ◽  
Shuo Wang ◽  
Ximena Paez-Colasante ◽  
Gary E. Landreth ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior ◽  
Neuromuscular Junctions ◽  
Germ Line ◽  
Fiber Type ◽  
Postnatal Growth ◽  
Mammalian Skeletal Muscle ◽  
Neuromuscular Synapses ◽  
Extracellular Signal

The Ras–extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway appears to be important for the development, maintenance, aging, and pathology of mammalian skeletal muscle. Yet no gene targeting ofErk1/2in muscle fibersin vivohas been reported to date. We combined a germ lineErk1mutation with Cre-loxPErk2inactivation in skeletal muscle to produce, for the first time, mice lacking ERK1/2 selectively in skeletal myofibers. Animals lacking muscle ERK1/2 displayed stunted postnatal growth, muscle weakness, and a shorter life span. Their muscles examined in this study, sternomastoid and tibialis anterior, displayed fragmented neuromuscular synapses and a mixture of modest fiber atrophy and loss but failed to show major changes in fiber type composition or absence of cell surface dystrophin. Whereas the lack of only ERK1 had no effects on the phenotypes studied, the lack of myofiber ERK2 explained synaptic fragmentation in the sternomastoid but not the tibialis anterior and a decrease in the expression of the acetylcholine receptor (AChR) epsilon subunit gene mRNA in both muscles. A reduction in AChR protein was documented in line with the above mRNA results. Evidence of partial denervation was found in the sternomastoid but not the tibialis anterior. Thus, myofiber ERK1/2 are differentially required for the maintenance of myofibers and neuromuscular synapses in adult mice.

scholarly journals Purification of desmin from adult mammalian skeletal muscle

1981 ◽  
Vol 195 (2) ◽  
pp. 345-356 ◽  
Author(s):  
J M O'Shea ◽  
R M Robson ◽  
M K Hartzer ◽  
T W Huiatt ◽  
W E Rathbun ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Average Diameter ◽  
Intermediate Filament Protein ◽  
Mammalian Skeletal Muscle ◽  
Cytoskeletal Function ◽  
10 Nm Filaments ◽  
And Function ◽  
Filament Protein

A method has been developed for preparation of purified desmin from mature mammalian (porcine) skeletal muscle. A crude desmin-containing fraction was prepared by modification of procedures used for isolation of smooth-muscle intermediate-filament protein [Small & Sobieszek (1977) J. Cell Sci. 23, 243-268]. The desmin was extracted in 1 M-acetic acid/20 mM-NaCl at 4 degrees C for 15h from the residue remaining after actomyosin extraction from washed myofibrils. Successive chromatography on hydroxyapatite and DEAE-Sepharose CL-6B in 6M-urea yielded desmin that was routinely more than 97% 55 000-dalton protein and that had no detectable actin contamination. Removal of urea by dialysis against 10mM-Tris/acetate (pH 8.5)/1 mM dithioerythritol and subsequent clarification at 134 000 g (rav. 5.9 cm) for 1 h results in a clear desmin solution. Dialysis of purified desmin against 100 mM-NaCl/1 mM-MgCl2/10 mM-imidazole/HCl, pH 7.0, at 2 degrees C resulted in the formation of synthetic desmin filaments have an average diameter of 9-11.5 nm. The present studies demonstrate that the relatively small amount of desmin in mature skeletal muscle can be isolated in sufficient quantity and purity to permit detailed studies of its properties and function. Although 10nm filaments have not been unequivocally demonstrated in mature muscle in vivo, that the purified skeletal-muscle desmin will form 10 nm filaments in vitro lends support to their possible existence and cytoskeletal function in mature skeletal-muscle cells.

scholarly journals Long-chain n-3 DHA reduces the extent of skeletal muscle fatigue in the rat in vivo hindlimb model

2013 ◽  
Vol 111 (6) ◽  
pp. 996-1003 ◽  
Author(s):  
Gregory E. Peoples ◽  
Peter L. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Fish Oil ◽  
Muscle Fatigue ◽  
Muscle Membrane ◽  
Mammalian Skeletal Muscle ◽  
Skeletal Muscle Fatigue ◽  
Arterial Blood ◽  
Oxygen Efficiency ◽  
Long Chain

Dietary fish oil modifies skeletal muscle membrane fatty acid composition and oxygen efficiency similar to changes in the myocardium. Oxygen efficiency is a key determinant of sustained force in mammalian skeletal muscle. Therefore, in the present study, we tested the effects of a fish-oil diet on skeletal muscle fatigue under the stress of contraction using the rat in vivo autologous perfused hindlimb model. For 8 weeks, male Wistar rats were fed a diet rich in saturated fat (SF), a diet rich in n-6 PUFA or a diet rich in long-chain (LC) n-3 PUFA DHA derived from fish oil. In anaesthetised, mechanically ventilated rats, with their hindlimbs perfused with arterial blood at a constant flow, the gastrocnemius–plantaris–soleus muscle bundle was stimulated via sciatic nerve (2 Hz, 6–12 V, 0·05 ms) to contract repetitively for 30 min. Rats fed the n-3 PUFA diet developed higher maximum twitch tension than those fed the SF and n-6 PUFA diets (P< 0·05) and sustained twitch tension through more repetitions before the tension declined to 50 % of the maximum twitch tension (P< 0·05). The n-3 PUFA group used less oxygen for tension developed and produced higher venous lactate concentrations with no difference in glycogen utilisation compared with the SF and n-6 PUFA groups. These results further support that incorporation of DHA into skeletal muscle membranes increases the efficiency of oxygen use over a range of contractile force and this is expressed as a higher sustained force and prolonged time to fatigue.

scholarly journals Fibro-adipogenic progenitors of dystrophic mice are insensitive to NOTCH regulation of adipogenesis

2019 ◽  
Vol 2 (3) ◽  
pp. e201900437 ◽  
Author(s):  
Milica Marinkovic ◽  
Claudia Fuoco ◽  
Francesca Sacco ◽  
Andrea Cerquone Perpetuini ◽  
Giulio Giuliani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Control Mechanism ◽  
Notch Pathway ◽  
Skeletal Muscle Regeneration ◽  
Wild Type ◽  
Adult Skeletal Muscle ◽  
Pathological Conditions ◽  
Dystrophic Mice

Fibro-adipogenic progenitors (FAPs) promote satellite cell differentiation in adult skeletal muscle regeneration. However, in pathological conditions, FAPs are responsible for fibrosis and fatty infiltrations. Here we show that the NOTCH pathway negatively modulates FAP differentiation both in vitro and in vivo. However, FAPs isolated from young dystrophin-deficient mdx mice are insensitive to this control mechanism. An unbiased mass spectrometry–based proteomic analysis of FAPs from muscles of wild-type and mdx mice suggested that the synergistic cooperation between NOTCH and inflammatory signals controls FAP differentiation. Remarkably, we demonstrated that factors released by hematopoietic cells restore the sensitivity to NOTCH adipogenic inhibition in mdx FAPs. These results offer a basis for rationalizing pathological ectopic fat infiltrations in skeletal muscle and may suggest new therapeutic strategies to mitigate the detrimental effects of fat depositions in muscles of dystrophic patients.

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