scholarly journals A Novel Conserved Isoform of the Ubiquitin Ligase UFD2a/UBE4B Is Expressed Exclusively in Mature Striated Muscle Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28861 ◽  
Author(s):  
Andrew L. Mammen ◽  
James A. Mahoney ◽  
Amanda St. Germain ◽  
Nisha Badders ◽  
J. Paul Taylor ◽  
...  
1984 ◽  
Vol 108 (1) ◽  
pp. 305-314
Author(s):  
B. L. BREZDEN ◽  
D. R. GARDNER

The mean resting potential in the heart ventricle muscle cells of the freshwater snail Lymnaea stagnalis was found to be −61.2±3.5 (˙˙) mV (ranging from −56mV to −68mV). The average intracellular potassium concentration was estimated to be 51.5±14.6(˙˙) m (ranging from 27.8 m to 77.3 m). The membrane of the heart ventricle muscle cells appears to be permeable to both potassium and chloride, as changes in the extracellular concentration of either of these ions resulted in a change in the membrane potential. A ten-fold change in the extracellular potassium concentration was associated with a 50.4±3.8(˙˙) mV slope when the potassium concentration was above about 6 m. Deviations from the straight-line relation predicted for a potassium electrode could be accounted for by introducing a term for sodium permeability. The ionic basis of the membrane potential in these cells can be described by a modified form of the Goldman-Hodgkin- Katz equation.


1971 ◽  
Vol 9 (1) ◽  
pp. 103-122
Author(s):  
R. B. KEMP ◽  
B. M. JONES ◽  
U. GRÖSCHEL-STEWART

Skeletal muscle and liver tissue from 9-day-old chick embryos were dissociated into separate cells using 0.25 % (w/v) crude trypsin. The effect of rabbit anti-actomyosin sera on the aggregation of these cells was estimated by the gyratory shaker and turbidimetric methods. Studies were also undertaken on the ability of fluorescein isothiocyanate-labelled rabbit anti-uterine actomyosin serum (FITC-labelled anti-UAM) to stain the cell surface and on the type specificity and species specificity of rabbit anti-chicken actomyosin sera. Antisera against chicken gizzard smooth-muscle actomyosin (anti-GAM) and against chicken pectoralis striated muscle actomyosin (anti-PAM) both gave single precipitin bands with their respective actomyosins on diffusion through agar. The antisera neither reacted with their heterologous actomyosin nor with gizzard tropomyosin; they were type-specific. Serial sections of human cervix were stained in a similar pattern with both anti-UAM and anti-GAM, showing that anti-smooth muscle actomyosin sera were not species-specific. The fibrocytes of the human umbilical cord and human platelets were stained by FITC-labelled anti-UAM serum but not by labelled anti-human PAM. The aggregation of muscle and liver cells over a 24-h period in the presence of antisera against human or chicken PAM was not significantly different from the controls incubated on a gyratory shaker in Eagle's minimum essential medium (MEM) containing 10% (v/v) rabbit non-immunized serum (NIS) or calf serum. However, anti-UAM and anti-GAM inhibited both the rate of aggregation of liver and muscle cells and the size of aggregates attained in 24 h. This effect could not be simulated with specific rabbit antisera against human plasma proteins. The globulin-enriched fraction of anti-GAM markedly inhibited the aggregation of liver and muscle cells in a range of concentrations between 50 and 500 µg per 2 x 106 cells/ml Eagle's MEM. In contrast, the aggregation of cells incubated with globulin-enriched anti-PAM was similar to the controls. The addition of anti-GAM globulins at 1 or 2 h to muscle cells rotated by the turbidimetric method reduced the aggregative competence of the cells over the remainder of a 4-h period. The possibility that the inhibitory effect of anti-UAM and anti-GAM on cell aggregation is due to impurities in the antisera or to a general reaction with cell surface ATPases is discussed but, in the light of evidence, rejected in favour of a reaction between the antisera and an actomyosin of the smooth-muscle type at the cell surface.


2020 ◽  
Author(s):  
Yansen Li ◽  
Mingfeng Fan ◽  
Hanxiang Le ◽  
Xiangjun Xu ◽  
Shuai Wang ◽  
...  

Abstract Background: Adipose-derived stem cells (ASCs) function in multi-directional differentiation, proliferation, and tissue regeneration. It is not clear whether microcarrier 6 can promote the migration, differentiation, and regeneration of fat stem cells, and improve therapeutic effects for the treatment of anal fistula.Methods: Japanese big ear rabbits were employed to establish an anal fistula model, and ASC-microcarrier 6 mixed transplantation was used as a treatment. HE staining, immunohistochemistry, and RNA sequencing were used to observe the effect of ASC-microcarrier 6 transplantation on anal fistula healing, in comparison with the ASC treatment group, rubber band operation group, and control group.Results: HE staining indicated scattered striated muscle cells and epithelial tissues in fistula tissues of the ASC-microcarrier 6 complex group and the ASC treatment group, while a small number of lymphocytes were clustered around the microcarrier 6, and fat cell aggregation was seen in the ASC treatment group. RNA sequence analysis showed that differential genes were mainly concentrated in striated muscle cells, vascular smooth muscle, and other tissues. PI3K/AKT signaling pathway molecules were significantly enriched, granulation tissue and lymphocyte infiltration were observed in the rubber band string operation group, and a large amount of necrotic tissue was seen in the control group.Conclusion: Microcarrier 6 is beneficial to the multi-directional differentiation of ASCs, which can provide a good environment for the survival of ASCs and promote fistula healing.


Author(s):  
Stanislas Bataille ◽  
Philippe Chauveau ◽  
Denis Fouque ◽  
Michel Aparicio ◽  
Laetitia Koppe

Abstract Chronic kidney disease (CKD) patients often exhibit a low muscle mass and strength, leading to physical impairment and an increased mortality. Two major signalling pathways control protein synthesis, the insulin-like growth factor-1/Akt (IGF-1/Akt) pathway, acting as a positive regulator, and the myostatin (Mstn) pathway, acting as a negative regulator. Mstn, also known as the growth development factor-8 (GDF-8), is a member of the transforming growth factor-β superfamily, which is secreted by mature muscle cells. Mstn inhibits satellite muscle cell proliferation and differentiation and induces a proteolytic phenotype of muscle cells by activating the ubiquitin–proteasome system. Recent advances have been made in the comprehension of the Mstn pathway disturbance and its role in muscle wasting during CKD. Most studies report higher Mstn concentrations in CKD and dialysis patients than in healthy subjects. Several factors increase Mstn production in uraemic conditions: low physical activity, chronic or acute inflammation and oxidative stress, uraemic toxins, angiotensin II, metabolic acidosis and glucocorticoids. Mstn seems to be only scarcely removed during haemodialysis or peritoneal dialysis, maybe because of its large molecule size in plasma where it is linked to its prodomain. In dialysis patients, Mstn has been proposed as a biomarker of muscle mass, muscle strength or physical performances, but more studies are needed in this field. This review outlines the interconnection between Mstn activation, muscle dysfunction and CKD. We discuss mechanisms of action and efficacy of pharmacological Mstn pathway inhibition that represents a promising treatment approach of striated muscle dysfunction. Many approaches and molecules are in development but until now, no study has proved a benefit in CKD.


1990 ◽  
Vol 32 (3) ◽  
pp. 317-322
Author(s):  
Shigeo Aiyama ◽  
Tomoyo Imamura ◽  
Seiji Takahashi ◽  
Hideki Furuya ◽  
Rie Ikeda ◽  
...  

2002 ◽  
Vol 88 (6) ◽  
pp. 3386-3397 ◽  
Author(s):  
Dan Rokni ◽  
Binyamin Hochner

The octopus arm provides a unique model for neuromuscular systems of flexible appendages. We previously reported the electrical compactness of the arm muscle cells and their rich excitable properties ranging from fast oscillations to overshooting action potentials. Here we characterize the voltage-activated ionic currents in the muscle cell membrane. We found three depolarization-activated ionic currents: 1) a high-voltage-activated L-type Ca2+ current, which began activating at approximately −35 mV, was eliminated when Ca2+ was substituted by Mg2+, was blocked by nifedipine, and showed Ca2+-dependent inactivation. This current had very rapid activation kinetics (peaked within milliseconds) and slow inactivation kinetics (τ in the order of 50 ms). 2) A delayed rectifier K+ current that was totally blocked by 10 mM TEA and partially blocked by 10 mM 4-aminopyridine (4AP). This current exhibited relatively slow activation kinetics (τ in the order of 15 ms) and inactivated only partially with a time constant of ∼150 ms. And 3) a transient A-type K+ current that was totally blocked by 10 mM 4AP and was partially blocked by 10 mM TEA. This current exhibited very fast activation kinetics (peaked within milliseconds) and inactivated with a time constant in the order of 60 ms. Inactivation of the A-type current was almost complete at −40 mV. No voltage-dependent Na+ current was found in these cells. The octopus arm muscle cells generate fast (∼3 ms) overshooting spikes in physiological conditions that are carried by a slowly inactivating L-type Ca2+ current.


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