scholarly journals Subcellular Specialization of Mitochondrial Form and Function in Skeletal Muscle Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
T. Bradley Willingham ◽  
Peter T. Ajayi ◽  
Brian Glancy
Keyword(s):  
Skeletal Muscle ◽  
Energy Homeostasis ◽  
Single Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Current Data ◽  
Skeletal Muscle Cells ◽  
Form And Function ◽  
Mitochondrial Heterogeneity ◽  
And Function

Across different cell types and within single cells, mitochondria are heterogeneous in form and function. In skeletal muscle cells, morphologically and functionally distinct subpopulations of mitochondria have been identified, but the mechanisms by which the subcellular specialization of mitochondria contributes to energy homeostasis in working muscles remains unclear. Here, we discuss the current data regarding mitochondrial heterogeneity in skeletal muscle cells and highlight potential new lines of inquiry that have emerged due to advancements in cellular imaging technologies.

scholarly journals Annexins and Membrane Repair Dysfunctions in Muscular Dystrophies

2021 ◽  
Vol 22 (10) ◽  
pp. 5276
Author(s):  
Coralie Croissant ◽  
Romain Carmeille ◽  
Charlotte Brévart ◽  
Anthony Bouter
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Genetic Disorders ◽  
Muscle Cells ◽  
Cell Types ◽  
Clinical Severity ◽  
Skeletal Muscle Cells ◽  
Muscular Dystrophies ◽  
Membrane Repair ◽  
Human Skeletal Muscle Cells

Muscular dystrophies constitute a group of genetic disorders that cause weakness and progressive loss of skeletal muscle mass. Among them, Miyoshi muscular dystrophy 1 (MMD1), limb girdle muscular dystrophy type R2 (LGMDR2/2B), and LGMDR12 (2L) are characterized by mutation in gene encoding key membrane-repair protein, which leads to severe dysfunctions in sarcolemma repair. Cell membrane disruption is a physiological event induced by mechanical stress, such as muscle contraction and stretching. Like many eukaryotic cells, muscle fibers possess a protein machinery ensuring fast resealing of damaged plasma membrane. Members of the annexins A (ANXA) family belong to this protein machinery. ANXA are small soluble proteins, twelve in number in humans, which share the property of binding to membranes exposing negatively-charged phospholipids in the presence of calcium (Ca2+). Many ANXA have been reported to participate in membrane repair of varied cell types and species, including human skeletal muscle cells in which they may play a collective role in protection and repair of the sarcolemma. Here, we discuss the participation of ANXA in membrane repair of healthy skeletal muscle cells and how dysregulation of ANXA expression may impact the clinical severity of muscular dystrophies.

scholarly journals Biosynthesis of titin in cultured skeletal muscle cells.

1989 ◽  
Vol 109 (5) ◽  
pp. 2189-2195 ◽  
Author(s):  
W B Isaacs ◽  
I S Kim ◽  
A Struve ◽  
A B Fulton
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Significant Progress ◽  
Large Protein ◽  
Time Period ◽  
And Function ◽  
Triton X ◽  
Developing Muscle ◽  
Synchronized Cultures

Although significant progress has been made regarding the structure and function of titin, little data exist on the biosynthesis of this large protein in developing muscle. Using pulse-labeling with [35S]methionine and immunoprecipitation with an anti-titin mAb, we have examined the biosynthesis of titin in synchronized cultures of skeletal muscle cells derived from day 12 chicken embryos. We find that: (a) titin synthesis increases greater than 4-fold during the first week in culture and during this same time period, synthesis of muscle-specific myosin heavy chain increases greater than 12-fold; (b) newly synthesized titin has a t1/2 of approximately 70 h; (c) titin is resistant to extraction with Triton X-100 both during and immediately after its synthesis. These observations suggest that newly synthesized titin molecules are stable proteins that rapidly associate with the cytoskeleton of developing myotubes.

scholarly journals Substrate utilisation of cultured skeletal muscle cells in patients with CFS

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Cara Tomas ◽  
Joanna L. Elson ◽  
Julia L. Newton ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Cultured Cells ◽  
Systemic Disease ◽  
Tca Cycle ◽  
Muscle Cells ◽  
Cell Types ◽  
Chronic Fatigue ◽  
Skeletal Muscle Cells ◽  
Flux Analysis ◽  
Healthy Controls

Abstract Chronic fatigue syndrome (CFS) patients often suffer from severe muscle pain and an inability to exercise due to muscle fatigue. It has previously been shown that CFS skeletal muscle cells have lower levels of ATP and have AMP-activated protein kinase dysfunction. This study outlines experiments looking at the utilisation of different substrates by skeletal muscle cells from CFS patients (n = 9) and healthy controls (n = 11) using extracellular flux analysis. Results show that CFS skeletal muscle cells are unable to utilise glucose to the same extent as healthy control cells. CFS skeletal muscle cells were shown to oxidise galactose and fatty acids normally, indicating that the bioenergetic dysfunction lies upstream of the TCA cycle. The dysfunction in glucose oxidation is similar to what has previously been shown in blood cells from CFS patients. The consistency of cellular bioenergetic dysfunction in different cell types supports the hypothesis that CFS is a systemic disease. The retention of bioenergetic defects in cultured cells indicates that there is a genetic or epigenetic component to the disease. This is the first study to use cells derived from skeletal muscle biopsies in CFS patients and healthy controls to look at cellular bioenergetic function in whole cells.

scholarly journals Tadalafil alters energy metabolism in C2C12 skeletal muscle cells.

2011 ◽  
Vol 58 (2) ◽  
Author(s):  
Stefania Sabatini ◽  
Paolo Sgrò ◽  
Guglielmo Duranti ◽  
Roberta Ceci ◽  
Luigi Di Luigi
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Energy Homeostasis ◽  
Citrate Synthase ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Cell Functions ◽  
C2c12 Skeletal Muscle Cells

Phosphodiesterases (PDEs) are a family of enzymes that hydrolyze cyclic nucleotides, thereby modulating cell functions. Three highly selective PDE5 inhibitors (PDE5i), sildenafil, vardenafil and tadalafil, have been developed for treatment of erectile dysfunction (ED). Experimental evidence showed that chronic treatment with sildenafil PDE5i in a mouse model of diet-induced obesity and insulin resistance improved insulin action and decreased circulating fatty acid levels. It has recently been shown that healthy athletes use PDE5i as performance enhancers, hence in the present study we investigated whether the long-lasting PDE5i tadalafil influences energy metabolism in C2C12 skeletal muscle cells by evaluating lactate production, glucose consumption, and citrate synthase and 3-OH acyl CoA dehydrogenase activities. Our data demonstrate that tadalafil is able to modulate energy homeostasis in mouse skeletal muscle cells, depending on the treatment length and dose.

scholarly journals Phosphorylation and function of DGAT1 in skeletal muscle cells

2015 ◽  
Vol 1 (1) ◽  
pp. 41-50 ◽  
Author(s):  
Jinhai Yu ◽  
Yiran Li ◽  
Fei Zou ◽  
Shimeng Xu ◽  
Pingsheng Liu
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
And Function

scholarly journals Immunohistochemical localization of annexin V (CaBP33) in rat organs.

1991 ◽  
Vol 39 (9) ◽  
pp. 1189-1198 ◽  
Author(s):  
I Giambanco ◽  
G Pula ◽  
P Ceccarelli ◽  
R Bianchi ◽  
R Donato
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Annexin V ◽  
Muscle Cells ◽  
Cell Types ◽  
Skeletal Muscle Cells ◽  
Secretory Cells ◽  
White Pulp ◽  
Rat Tissues ◽  
Peritubular Capillaries

We investigated the cellular distribution of annexin V (CaBP33) in rat tissues by immunohistochemistry. Several cell types were shown to express the protein. Glial cells in the cerebellum and in the optic nerve, the corneal epithelium, the posterior epithelium in the iris, chondrocytes, skeletal muscle cells and cardiomyocytes, the capillary endothelial cells in many organs, the muscularis mucosae and the muscular layer in the intestinal tract, hepatocytes, Müller cells in the retina, the lens fibers, Sertoli and Leydig cells in the testis, and smooth muscle cells in the epididymis and bronchi displayed intense immunostaining. In the adrenal gland, only the cortex showed immunoreaction product. In the kidney, no apparent staining of renal cells was observed, whereas endothelial cells of peritubular capillaries were stained. In the heart, annexin V was found associated exclusively with the sarcolemma and intercalated discs, as opposed to the diffuse distribution of the protein in skeletal muscle cells. In the spleen, only reticular elements in the white pulp and endothelial cells in the red pulp appeared to be immunostained. The present data complement the biochemical work thus far done on annexin V and suggest that the protein is neither restricted to secretory cells nor exclusively related to exocytotic events in secretory cells.

scholarly journals Toxic Effect of Vancomycin on Viability and Functionality of Different Cells Involved in Tissue Regeneration

Antibiotics ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 238
Author(s):  
Joy Braun ◽  
Stefanie Eckes ◽  
Pol Maria Rommens ◽  
Katja Schmitz ◽  
Daniela Nickel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Toxic Effect ◽  
Tissue Regeneration ◽  
Bone Fractures ◽  
Muscle Cells ◽  
High Serum ◽  
Host Cells ◽  
Skeletal Muscle Cells ◽  
High Concentrations ◽  
And Function

To prevent infections local delivery of antibiotics is a useful tool. Especially in bone fractures, vancomycin impregnated bone cements are often used allowing high concentrations of antibiotics at the infection side without high serum concentrations. However, besides potential pathogens, cells involved in tissue regeneration may also be affected by the drug. We investigated the effect of vancomycin on the viability and functionality on osteoblasts, endothelial cells, fibroblasts and skeletal muscle cells. Our results show that the viability of all cells analyzed was reduced by vancomycin and that the observed effects were time and concentration dependent. The most pronounced toxic effect was detected on day three when even the lowest concentration of 0.01 mg/ml led to a significant decrease in proliferation compared to control. Functionality assays of osteoblasts and skeletal muscle cells revealed a sensitive reaction of the cells to the drug, indicating that vancomycin is toxic to these cells during the process of differentiation. These data suggest that the vancomycin administration is critical for cell survival and function. Therefore, the concentration of administered antibiotics needs to be carefully evaluated to find a balance between defense against pathogens and functionality of host cells and tissues.

scholarly journals Regulation of Lin28a-miRNA let-7b-5p pathway in skeletal muscle cells by peroxisome proliferator-activated receptor delta

2020 ◽  
Vol 319 (3) ◽  
pp. C541-C551
Author(s):  
Hygor N. Araujo ◽  
Tanes I. Lima ◽  
Dimitrius Santiago P. S. F. Guimarães ◽  
Andre G. Oliveira ◽  
Bianca C. Favero-Santos ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Homeostasis ◽  
Muscle Cells ◽  
C2c12 Cells ◽  
Skeletal Muscle Cells ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Primary Mouse ◽  
Murine Skeletal Muscle ◽  
Muscle Biopsies

Lin28a/miRNA let-7b-5p pathway has emerged as a key regulators of energy homeostasis in the skeletal muscle. However, the mechanism through which this pathway is regulated in the skeletal muscle has remained unclear. We have found that 8 wk of aerobic training (Tr) markedly decreased let-7b-5p expression in murine skeletal muscle, whereas high-fat diet (Hfd) increased its expression. Conversely, Lin28a expression, a well-known inhibitor of let-7b-5p, was induced by Tr and decreased by Hfd. Similarly, in human muscle biopsies, Tr increased LIN28 expression and decreased let-7b-5p expression. Bioinformatics analysis of LIN28a DNA sequence revealed that its enrichment in peroxisome proliferator-activated receptor delta (PPARδ) binding sites, which is a well-known metabolic regulator of exercise. Treatment of primary mouse skeletal muscle cells or C2C12 cells with PPARδ activators GW501516 and AICAR increased Lin28a expression. Lin28a and let-7b-5p expression was also regulated by PPARδ coregulators. While PPARγ coactivator-1α (PGC1α) increased Lin28a expression, corepressor NCoR1 decreased its expression. Furthermore, PGC1α markedly reduced the let-7b-5p expression. PGC1α-mediated induction of Lin28a expression was blocked by the PPARδ inhibitor GSK0660. In agreement, Lin28a expression was downregulated in PPARδ knocked-down cells leading to increased let-7b-5p expression. Finally, we show that modulation of the Lin28a- let-7b-5p pathway in muscle cells leads to changes in mitochondrial metabolism in PGC1α dependent fashion. In summary, we demonstrate that Lin28a- let-7b-5p is a direct target of PPARδ in the skeletal muscle, where it impacts mitochondrial respiration.

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