Chronic treatment with D600 enhances development of sodium channels in cultured chick skeletal muscle cells

1992 ◽  
Vol 138 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Ryohei Satoh ◽  
Yumiko Nakabayashi ◽  
Masaakira Kano
Keyword(s):  
Skeletal Muscle ◽  
Sodium Channels ◽  
Chronic Treatment ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

scholarly journals Thermotherapy Effects on Healthy and Type 2 Diabetes Human Skeletal Muscle Myoblast Cell Lines

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Janette A. Lindstrom ◽  
Felix Omoruyi ◽  
Jean Sparks
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Cell Lines ◽  
Acute Treatment ◽  
Human Skeletal Muscle ◽  
Chronic Treatment ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

Diabetes mellitus is a chronic metabolic disease characterized by elevated blood glucose levels with associated disordered carbohydrate and lipid metabolism. Type 2 diabetes (T2D) specifically has been shown to cause a decrease in skeletal muscle mass due to oxidative stress. This study investigated a treatment option for T2D through thermotherapy on healthy (HSMM) and T2D (D-HSMM) human skeletal muscle cells. The goals were to determine the effects of thermotherapy, long-term (chronic) and short-term (acute), on HSMM and D-HSMM cell viabilities and oxidative stress. HSMM and D-HSMM cells were grown to confluency, harvested, and counted to determine density. Acute and chronic heat treatments were applied to both cell lines. The chronic treatment consisted of a 30-minute exposure to 40°C, three times a week for three weeks; the acute treatment was a one-time exposure. Oxidative stress assays and cell viabilities were tested 24 hours after heat treatments. Results indicated no significant effect on the cell viability of HSMM and D-HSMM cells. The acute treatment had a significant increase ( p ≤ 0.05 ) of MDA concentration compared to the chronic treatment. The chronic treatment had a significant increase ( p ≤ 0.05 ) in catalase activity compared to the acute treatment. The SOD activity had no significant change ( p > 0.05 ) between the chronic and acute treatments. In conclusion, acute thermotherapy may not be beneficial for skeletal muscle cells due to the observed increase in oxidative stress, especially in the D-HSMM cells.

Extracts of Hymenocardia acida ameliorate insulin resistance in skeletal muscle cells

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
II Ezeigbo ◽  
C Wheeler-Jones ◽  
S Gibbons ◽  
ME Cleasby
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Ameliorate Insulin Resistance

TGFß regulates metabolism of human skeletal muscle cells by miRNAs

2018 ◽  
Author(s):  
S Höckele ◽  
P Huypens ◽  
C Hoffmann ◽  
T Jeske ◽  
M Hastreiter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Human Skeletal Muscle Cells

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.

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