scholarly journals Skeletal muscle-on-a-chip: an in vitro model to evaluate tissue formation and injury

Lab on a Chip ◽  
2017 ◽  
Vol 17 (20) ◽  
pp. 3447-3461 ◽  
Author(s):  
Gaurav Agrawal ◽  
Aereas Aung ◽  
Shyni Varghese

We introduce a microfluidic platform in which we culture three-dimensional skeletal muscle tissues, while evaluating tissue formation and toxin-induced muscle injury.

2020 ◽  
Vol 4 (11) ◽  
pp. 2000121
Author(s):  
Takunori Nagashima ◽  
Stacy Hadiwidjaja ◽  
Saki Ohsumi ◽  
Akari Murata ◽  
Takumi Hisada ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0232081 ◽  
Author(s):  
Anna Urciuolo ◽  
Elena Serena ◽  
Rusha Ghua ◽  
Susi Zatti ◽  
Monica Giomo ◽  
...  

Rheumatology ◽  
2019 ◽  
Vol 59 (1) ◽  
pp. 224-232
Author(s):  
Mari Kamiya ◽  
Fumitaka Mizoguchi ◽  
Akito Takamura ◽  
Naoki Kimura ◽  
Kimito Kawahata ◽  
...  

Abstract Objectives The hallmark histopathology of PM is the presence of CD8+ T cells in the non-necrotic muscle cells. The aim of this study was to clarify the pathological significance of CD8+ T cells in muscle cells. Methods C2C12 cells were transduced retrovirally with the genes encoding MHC class I (H2Kb) and SIINFEKL peptide derived from ovalbumin (OVA), and then differentiated to myotubes (H2KbOVA-myotubes). H2KbOVA-myotubes were co-cultured with OT-I CD8+ T cells derived from OVA-specific class I restricted T cell receptor transgenic mice as an in vitro model of PM to examine whether the CD8+ T cells invade into the myotubes and if the myotubes with the invasion are more prone to die than those without. Muscle biopsy samples from patients with PM were examined for the presence of CD8+ T cells in muscle cells. The clinical profiles were compared between the patients with and without CD8+ T cells in muscle cells. Results Analysis of the in vitro model of PM with confocal microscopy demonstrated the invasion of OT-I CD8+ T cells into H2KbOVA-myotubes. Transmission electron microscopic analysis revealed an electron-lucent area between the invaded CD8+ T cell and the cytoplasm of H2KbOVA-myotubes. The myotubes invaded with OT-I CD8+ T cells died earlier than the uninvaded myotubes. The level of serum creatinine kinase was higher in patients with CD8+ T cells in muscle cells than those without these cells. Conclusion CD8+ T cells invade into muscle cells and contribute to muscle injury in PM. Our in vitro model of PM is useful to examine the mechanisms underlying muscle injury induced by CD8+ T cells.


Author(s):  
Valerie A. Cwik ◽  
Ramanath Majumdar ◽  
Michael H. Brooke

Abstract:An in vitro model of muscle damage was used to investigate the protective effect of mild hypothermia in muscle injury. Rat epitrochlearis muscles were dissected in their entirety and suspended in Krebs-Ringer solution and DNP, a mitochondrial uncoupler, was added. PGE2, and lactate release and the contractile response to stimulation were measured and compared to untreated controls. Experiments were done at 37, 35, 33 and 27°C. At 37°C, DNP stimulated muscle releases large amounts of PGE2and lactate and is unable to contract. As the temperature is reduced, there is progressive preservation of contractile force, although high lactate levels at the lowest temperatures indicate that the metabolic stress is still present. In contrast, DNP stimulated PGE2release is completely inhibited at or below 35°C and may be related to a similar protective phenomenon seen in experimental ischemic neuronal death.


Leukemia ◽  
2019 ◽  
Vol 34 (1) ◽  
pp. 271-282 ◽  
Author(s):  
Edda María Elvarsdóttir ◽  
Teresa Mortera-Blanco ◽  
Marios Dimitriou ◽  
Thibault Bouderlique ◽  
Monika Jansson ◽  
...  

2014 ◽  
Vol 5 ◽  
pp. 204173141454418 ◽  
Author(s):  
Tarig Magdeldin ◽  
Víctor López-Dávila ◽  
Cecile Villemant ◽  
Grant Cameron ◽  
Rosemary Drake ◽  
...  

1997 ◽  
Vol 138 (6) ◽  
pp. 1323-1331 ◽  
Author(s):  
Ann Redfield ◽  
Marvin T. Nieman ◽  
Karen A. Knudsen

The cell–cell adhesion molecule N-cadherin, with its associated catenins, is expressed by differentiating skeletal muscle and its precursors. Although N-cadherin's role in later events of skeletal myogenesis such as adhesion during myoblast fusion is well established, less is known about its role in earlier events such as commitment and differentiation. Using an in vitro model system, we have determined that N-cadherin– mediated adhesion enhances skeletal muscle differentiation in three-dimensional cell aggregates. We transfected the cadherin-negative BHK fibroblastlike cell line with N-cadherin. Expression of exogenous N-cadherin upregulated endogenous β-catenin and induced strong cell–cell adhesion. When BHK cells were cultured as three-dimensional aggregates, N-cadherin enhanced withdrawal from the cell cycle and stimulated differentiation into skeletal muscle as measured by increased expression of sarcomeric myosin and the 12/101 antigen. In contrast, N-cadherin did not stimulate differentiation of BHK cells in monolayer cultures. The effect of N-cadherin was not unique since E-cadherin also increased the level of sarcomeric myosin in BHK aggregates. However, a nonfunctional mutant N-cadherin that increased the level of β-catenin failed to promote skeletal muscle differentiation suggesting an adhesion-competent cadherin is required. Our results suggest that cadherin-mediated cell–cell interactions during embryogenesis can dramatically influence skeletal myogenesis.


2014 ◽  
Vol 10 (11) ◽  
pp. 4742-4749 ◽  
Author(s):  
Abigail C. Parks ◽  
Kevin Sung ◽  
Benjamin M. Wu

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