P2.21 Dysferlin-mediated membrane repair system contributes to maintenance of skeletal muscle cell viability in mouse models for muscular dystrophy

2011 ◽  
Vol 21 (9-10) ◽  
pp. 667
Author(s):  
T. Toda ◽  
M. Kanagawa ◽  
Z. Lu ◽  
C. Ito ◽  
A. Kuga ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Cell Viability ◽  
Mouse Models ◽  
Muscle Cell ◽  
Skeletal Muscle Cell ◽  
Repair System ◽  
Membrane Repair

scholarly journals ViaFuse: Fiji macros to calculate skeletal muscle cell viability and fusion index

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Emma Rose Hinkle ◽  
Tasneem Omar Essader ◽  
Gabrielle Marie Gentile ◽  
Jimena Giudice
Keyword(s):  
Skeletal Muscle ◽  
Cell Viability ◽  
Muscle Cell ◽  
Mathematical Knowledge ◽  
Skeletal Muscle Cell ◽  
Biological Features ◽  
Analysis Process ◽  
Actin Protein ◽  
Intuitive Interface ◽  
High Degree

Abstract Background Measuring biological features of skeletal muscle cells is difficult because of their unique morphology and multinucleate nature upon differentiation. Here, we developed a new Fiji macro package called ViaFuse (that stands for viability and fusion) to measure skeletal muscle cell viability and differentiation. To test ViaFuse, we utilized immunofluorescence images of differentiated myotubes where the capping actin protein of muscle z-line subunit beta (CAPZB) was depleted in comparison with control cells. Results We compared the values achieved using the ViaFuse macros first with manual quantification performed by researchers and second with those obtained utilizing the MATLAB muscle-centric software MyoCount. We observed a high degree of correlation between all methods of quantification. Conclusions ViaFuse can detect the borders of myotubes and identify nuclear clumps which have been limitations of previous muscle-centric imaging software. The ViaFuse macros require little computer power or space to run and user inputs to the ViaFuse macros are minimal, thereby automating the analysis process in a quick, easy, and accurate fashion. Additionally, the ViaFuse macros work with Fiji, an existing imaging software widely used by skeletal muscle researchers. Furthermore, ViaFuse is compatible with many computer systems, has a very intuitive interface, and does not require prior complex mathematical knowledge. Therefore, we propose ViaFuse as a robust and meticulous method to quantify skeletal muscle cell viability and differentiation.

scholarly journals The Effect of Acute and Chronic Thermotherapy on Type 2 Diabetic Skeletal Muscle Gene Expression and Inflammatory Markers

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1276
Author(s):  
Louay Bachnak ◽  
Jean Sparks ◽  
Daniel E. Newmire ◽  
Xavier F. Gonzales ◽  
Felix O. Omoruyi
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Cell Viability ◽  
Cell Lines ◽  
Muscle Cell ◽  
Skeletal Muscle Cell ◽  
Muscle Gene Expression ◽  
Tnf Α ◽  
Muscle Gene

Background: Type 2 diabetes (T2D) is a chronic illness associated with resistance to or defective insulin secretion. This study investigates the effects of thermotherapy on cell viability, gene expression and inflammation in skeletal muscle cell lines. Methods: Healthy and T2D human skeletal muscle cell lines (HSMM and D-HSMM, respectively) were subjected to acute or chronic thermo-therapy (AT or CT, respectively). CT consisted of a 30 min exposure to 40 °C, three times a week for three weeks; AT was a one-time exposure. Results: A significant decrease in D-HSMM cell viability percentage followed AT; however, no significant change occurred in CT. HSMM yielded the highest elevations of genes following CT. In D-HSMM, both treatments yielded gene upregulation. Both treatments significantly down-regulated IL-1β, IL-6, IL-10 and TNF-α in HSMM. AT significantly decreased IL-1β, IL-6 and upregulated IL-10 and TNF-α levels in D-HSMM, while CT yielded a reduction in IL-4, TNF-α and an upregulation of IL-6 and IL-10. Conclusions: An increase in gene expression indicates actin activity and cellular responses, suggesting an increase in transcriptional regulation. The upregulation of IL-6 and IL-10 in D-HSMM negatively correlated with a decrease in TNF-α and IL-1β, indicating improved adverse inflammatory effects associated with the disease.

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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