scholarly journals 4Hz mechanical vibration relieves pain through Na+/K+-ATPase α3 isoform-dependent brain tissue dehydration

2017 ◽  
Vol 6 (2) ◽  
pp. 29
Author(s):  
Gohar Musheghyan ◽  
Arevik Minasyan ◽  
Gohar Arajyan ◽  
Sinerik Ayrapetyan
Keyword(s):  
Brain Tissue ◽  
Muscle Tissue ◽  
Heart Muscle ◽  
Pain Threshold ◽  
Mechanical Vibration ◽  
Membrane Receptors ◽  
Tissue Hydration ◽  
Thermal Pain ◽  
Muscle Tissues

In this work the effect of 4Hz 30dB horizontal mechanical vibration (MV) on thermal pain threshold, hydration and [3H]-ouabain binding in brain and heart muscle tissues of rats was studied. It was revealed that 4Hz MV treatment for 10 minutes increased pain threshold, which was accompanied by brain and heart muscle tissue dehydration. In vitro state, hydration of brain and heart muscle tissues of sham animals was increased, while in 4Hz MV-treated animals the increase of brain tissue hydration was more pronounced and heart muscle tissues were dehydrated. The fact that 4Hz MV treatment also impacted heart muscle tissue hydration indicates that 4Hz MV effect on brain and heart muscle tissues is realized through a common messenger circulating in blood. The incubation of brain and heart muscle tissues in PS containing 10-4M and 10-9M ouabain led to tissue hydration in sham and 4Hz MV-treated animals. However, tissues of 4Hz MV-treated animals were less hydrated, and this hydration was accompanied by the decrease and increase of membrane receptors’ affinity at 10-4M and 10-9M ouabain concentrations, respectively. Based on the obtained data, it is suggested that pain-relieving effect of 4Hz MV is due to α3 isoform-dependent brain tissue dehydration.

scholarly journals A Cylindrical Molding Method for the Biofabrication of Plane-Shaped Skeletal Muscle Tissue

Micromachines ◽  
2021 ◽  
Vol 12 (11) ◽  
pp. 1411
Author(s):  
Minghao Nie ◽  
Ai Shima ◽  
Kenta Fukushima ◽  
Yuya Morimoto ◽  
Shoji Takeuchi
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Myogenic Differentiation ◽  
Skeletal Muscle Tissue ◽  
Differentiation Markers ◽  
Animal Products ◽  
Molding Method ◽  
Muscle Tissues ◽  
Central Pillar

Muscle tissues can be fabricated in vitro by culturing myoblast-populated hydrogels. To counter the shrinkage of the myoblast-populated hydrogels during culture, a pair of anchors are generally utilized to fix the two ends of the hydrogel. Here, we propose an alternative method to counter the shrinkage of the hydrogel and fabricate plane-shaped skeletal muscle tissues. The method forms myoblast-populated hydrogel in a cylindrical cavity with a central pillar, which can prevent tissue shrinkage along the circumferential direction. By eliminating the usages of the anchor pairs, our proposed method can produce plane-shaped skeletal muscle tissues with uniform width and thickness. In experiments, we demonstrate the fabrication of plane-shaped (length: ca. 10 mm, width: 5~15 mm) skeletal muscle tissue with submillimeter thickness. The tissues have uniform shapes and are populated with differentiated muscle cells stained positive for myogenic differentiation markers (i.e., myosin heavy chains). In addition, we show the assembly of subcentimeter-order tissue blocks by stacking the plane-shaped skeletal muscle tissues. The proposed method can be further optimized and scaled up to produce cultured animal products such as cultured meat.

scholarly journals Electrophysiological analysis of healthy and dystrophic 3D bioengineered skeletal muscle tissues

2021 ◽  
Author(s):  
Christine T. Nguyen ◽  
Majid Ebrahimi ◽  
Penney M. Gilbert ◽  
Bryan Andrew Stewart
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cell ◽  
Muscle Tissue ◽  
Three Dimensional ◽  
Dystrophin Gene ◽  
Muscle System ◽  
Electrophysiological Analysis ◽  
Cytoskeletal Network ◽  
Muscle Tissues

Recently, methods for creating three-dimensional (3D) human skeletal muscle tissues from myogenic cell lines have been reported. Bioengineered muscle tissues are contractile and respond to electrical and chemical stimulation. In this study we provide an electrophysiological analysis of healthy and dystrophic 3D bioengineered skeletal muscle tissues. We focus on Duchenne muscular dystrophy (DMD), a fatal muscle disorder involving the skeletal muscle system. The dystrophin gene, which when mutated causes DMD, encodes for the Dystrophin protein, which anchors the cytoskeletal network inside of a muscle cell to the extracellular matrix outside the cell. Here, we enlist a 3D in vitro model of DMD muscle tissue, to evaluate an understudied aspect of DMD, muscle cell electrical properties uncoupled from presynaptic neural inputs. Our data shows that electrophysiological aspects of DMD are replicated in the 3D bioengineered skeletal muscle tissue model. Furthermore, we test a block co-polymer, poloxamer 188, and demonstrate capacity for improving the membrane potential in DMD muscle. Therefore, this study serves as the baseline for a new in vitro method to examine potential therapies directed at muscular disorders.

Lipid peroxidation of skeletal muscle: an in vitro study

1983 ◽  
Vol 3 (7) ◽  
pp. 609-619 ◽  
Author(s):  
M. J. Jackson ◽  
D. A. Jones ◽  
R. H. T. Edwards
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Free Radical ◽  
Vitamin E ◽  
Hydroxyl Radicals ◽  
Muscle Tissue ◽  
In Vitro Study ◽  
Muscle Tissues ◽  
In Vitro Technique

The process of lipid peroxidation of skeletal muscle has been examined in vitro by monitoring the autoxidation of skeletal-muscle homogenates. Skeletal-muscle tissue has been shown to have considerable capacity for autoxidation and the process has been found to be initiated by a free-radical-mediated mechanism, critically dependent on the presence of free iron in the homogenate. The initiating radicals have not been firmly identified, but the results suggest that neither superoxide or hydroxyl radicals are involved. An in vitro technique for assessment of the antioxidant capacity of muscle tissue has also been developed which is capable of demonstrating differences between muscle tissues with differing vitamin E contents.

scholarly journals SGK1 Inhibits Autophagy in Murine Muscle Tissue

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Theresia Zuleger ◽  
Julia Heinzelbecker ◽  
Zsuzsanna Takacs ◽  
Catherine Hunter ◽  
Jakob Voelkl ◽  
...  
Keyword(s):  
Muscle Tissue ◽  
White Muscle ◽  
Autophagic Flux ◽  
Tissue Extracts ◽  
Muscle Tissues ◽  
Red Muscle ◽  
Autophagic Degradation

Background/Aims. As autophagy is linked to several pathological conditions, like cancer and neurodegenerative diseases, it is crucial to understand its regulatory signaling network. In this study, we investigated the role of the serum- and glucocorticoid-induced protein kinase 1 (SGK1) in the control of autophagy. Methods. To measure autophagic activity in vivo, we quantified the abundance of the autophagy conjugates LC3-PE (phosphatidylethanolamine) and ATG12-ATG5 in tissue extracts of SGK1 wild-type (Sgk1+/+) and knockout (Sgk1−/−) mice that were either fed or starved for 24 h prior sacrifice. In vitro, we targeted SGK1 by RNAi using GFP-WIPI1 expressing U-2 OS cells to quantify the numbers of cells displaying newly formed autophagosomes. In parallel, these cells were also assessed with regard to LC3 and ULK1 by quantitative Western blotting. Results. The abundance of both LC3-PE (LC3-II) and ATG12-ATG5 was significantly increased in red muscle tissues of SGK1 knockout mice. This was found in particular in fed conditions, suggesting that SGK1 may keep basal autophagy under control in red muscle in vivo. Under starved conditions, significant differences were observed in SGK1-deficient white muscle tissue and, under fed conditions, also in the liver. In vitro, we found that SGK1 silencing provoked a significant increase of cells displaying WIPI1-positive autophagosomes and autophagosomal LC3 (LC3-II). Moreover, autophagic flux assessments revealed that autophagic degradation significantly increased in the absence of SGK1, strongly suggesting that SGK1 inhibits both autophagosome formation and autophagic degradation in vitro. In addition, more ULK1 protein lacking the inhibitory, TORC1-specific phosphorylation at serine 758 was detected in the absence of SGK1. Conclusions. Combined, our data strongly support the idea that SGK1 inhibits the process of autophagy. Mechanistically, our data suggest that SGK1 should act upstream of ULK1 in regulating autophagy, and we hypothesize that SGK1 contributes to the regulation of ULK1 gene expression.

scholarly journals Plasma and tissue concentrations of α-tocopherol during vitamin E depletion in sheep

1993 ◽  
Vol 69 (1) ◽  
pp. 225-232 ◽  
Author(s):  
J. M. Fry ◽  
G. M. Smith ◽  
M. C Mcgrath ◽  
E. J. Speijers ◽  
J. G. Allen
Keyword(s):  
Adipose Tissue ◽  
Vitamin E ◽  
Heart Muscle ◽  
Skeletal Muscles ◽  
Experimental Conditions ◽  
Deficient Diet ◽  
Tocopherol Concentration ◽  
Muscle Tissues ◽  
The Relationship

To determine the relationship between plasma and tissue α-tocopherol concentrations during vitamin E depletion, weaned lambs were placed on a vitamin E-deficient diet for 0, 1, 2, 4, 8 and 12 weeks. α-Tocopherol was measured in plasma, erythrocytes, liver, adrenal, adipose tissue, three different skeletal muscles and heart muscle. The α-tocopherol concentration in plasma fell at the same rate as the α-tocopherol concentration in skeletal muscles, heart muscle, adrenal and adipose tissue. The α-tocopherol concentration in liver and erythrocytes fell at a faster rate than that of plasma and all muscle tissues. There were significant correlations between α-tocopherol concentration in plasma and α-tocopherol concentrations in all the tissues measured. Different skeletal muscles had significantly different concentrations of α-tocopherol which may relate to their differing susceptibility to nutritional myopathy. The increase in malondialdehyde in oxidatively-stressed muscle tissue and the correlation with α-tocopherol concentration in most muscle tissues indicated that the muscles had reduced antioxidant capacityin vitroas a result of vitamin E depletion. It was concluded that during vitamin E depletion in sheep α-tocopherol concentration in plasma was a good index of vitamin E status under the experimental conditions employed.

scholarly journals Electrophysiological analysis of healthy and dystrophic 3D bioengineered skeletal muscle tissues

2020 ◽  
Author(s):  
Christine T Nguyen ◽  
Majid Ebrahmi ◽  
Penney M Gilbert ◽  
Bryan A Stewart
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cell ◽  
Muscle Tissue ◽  
Three Dimensional ◽  
Muscle System ◽  
Electrophysiological Analysis ◽  
Cytoskeletal Network ◽  
Muscle Tissues ◽  
Dystrophin Protein

AbstractRecently, methods for creating three-dimensional (3D) human skeletal muscle tissues from myogenic cell lines have been reported. Bioengineered muscle tissues are contractile and respond to electrical and chemical stimulation. In this study we provide an electrophysiological analysis of healthy and dystrophic 3D bioengineered skeletal muscle tissues. We focus on Duchenne muscular dystrophy (DMD), a fatal muscle disorder involving the skeletal muscle system. The dystrophin gene, which when mutated causes DMD, encodes for the Dystrophin protein, which anchors the cytoskeletal network inside of a muscle cell to the extracellular matrix outside the cell. Here, we enlist a 3D in vitro model of DMD muscle tissue, to evaluate an understudied aspect of DMD, muscle cell electrical properties uncoupled from presynaptic neural inputs. Our data shows that electrophysiological aspects of DMD are replicated in the 3D bioengineered skeletal muscle tissue model. Furthermore, we test a block co-polymer, poloxamer 188, and demonstrate capacity for improving the membrane potential in DMD muscle.Therefore, this study serves as the baseline for a new in vitro method to examine potential therapies directed at muscular disorders.

SENSITIVITY OF THE RAT DIAPHRAGM TO GROWTH HORMONE.

1967 ◽  
Vol 54 (4) ◽  
pp. 645-662 ◽  
Author(s):  
Å. Hjalmarson ◽  
K. Ahrén
Keyword(s):  
Growth Hormone ◽  
Inhibitory Effect ◽  
Rat Diaphragm ◽  
Intracellular Accumulation ◽  
Slight Effect ◽  
Kidney Capsule ◽  
Muscle Tissues ◽  
Hypophysectomized Rats ◽  
Isolated Rat

ABSTRACT The effect of growth hormone (GH) in vitro on the rate of intracellular accumulation of the non-utilizable amino acid α-aminoisobutyric acid (AIB) was studied in the intact rat diaphragm preparation. Bovine or ovine GH (25 μg/ml incubation medium) markedly stimulated the accumulation of AIB-14C by diaphragms from hypophysectomized rats, while there was no or only a very slight effect on diaphragms from normal rats. In diaphragms from rats with the pituitary gland autotransplanted to the kidney capsule GH in vitro stimulated the accumulation of AIB-14C significantly more than in diaphragms from normal rats but significantly less than in diaphragms from hypophysectomized rats. Injections of GH intramuscularly for 4 days to hypophysectomized rats made the diaphragms from these rats less sensitive or completely insensitive to GH in vitro. These results indicate strongly that the relative insensitivity to GH in vitro of diaphragms from normal rats is due to the fact that the muscle tissues from these rats has been exposed to the endogenously secreted GH. The results show that GH can influence the accumulation of AIB-14C in the isolated rat diaphragm in two different ways giving an acute or »stimulatory« effect and a late or »inhibitory« effect, and that it seems to be a time-relationship between these two effects of the hormone.

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