Full metadata
Title
Using mechanical strain as a vehicle to direct fibroblasts-mediated myoblast differentiation and myotube function
Description
Skeletal muscle injury may occur from repetitive short bursts of biomechanical strain that impair muscle function. Alternatively, variations of biomechanical strain such as those held for long-duration are used by clinicians to repair muscle and restore its function. Fibroblasts embedded within the unifying connective tissue of skeletal muscle experience these multiple and diverse mechanical stimuli and respond by secreting cytokines. Cytokines direct all stages of muscle regeneration including myoblasts differentiation, fusion to form myotubes, and myotube functionality. To examine how fibroblasts respond to variations in mechanical strain that may affect juxtapose muscle, a myofascial junction was bioengineered that examined the interaction between the two cell types. Fibroblasts were experimentally shown to increase myoblast differentiation, and fibroblast biomechanical strain mediated the extent to which differentiation occurred. Intereleukin-6 is a strain-regulated cytokine secreted by fibroblasts was determined to be necessary for fibroblast-mediated myoblast differentiation. Myotubes differentiated in the presence of strained fibroblasts express greater number of acetylcholine receptors, greater acetylcholine receptor sizes, and modified to be more or less sensitive to acetylcholine-induced contraction. This study provides direct evidence that strained and non-strained fibroblasts can serve as a vehicle to modify myoblast differentiation and myotube functionality. Further understanding the mechanisms regulating these processes may lead to clinical interventions that include strain-activated cellular therapies and bioengineered cell engraftment for mediating the regeneration and function of muscle in vivo.
Date Created
2014
Contributors
- Hicks, Michael (Author)
- Standley, Paul R (Thesis advisor)
- Rawls, Jeffrey (Committee member)
- Lake, Douglas (Committee member)
- Hinrichs, Richard (Committee member)
- Arizona State University (Publisher)
Topical Subject
Resource Type
Extent
vi, 115 p. : ill. (some col.)
Language
Copyright Statement
In Copyright
Primary Member of
Peer-reviewed
No
Open Access
No
Handle
https://hdl.handle.net/2286/R.I.25887
Statement of Responsibility
by Michael Hicks
Description Source
Retrieved on Nov. 26, 2014
Level of coding
full
Note
Partial requirement for: Ph.D., Arizona State University, 2014
Note type
thesis
Includes bibliographical references (p. 91-98)
Note type
bibliography
Field of study: Molecular and cellular biology
System Created
- 2014-10-01 05:06:13
System Modified
- 2021-08-30 01:32:59
- 3 years ago
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