Growth Factors for Skeletal Muscle Tissue Engineering

Syverud, Brian C; VanDusen, Keith W.; Larkin, Lisa M.

doi:10.1159/000444671

Cited by 60 publications

(45 citation statements)

References 57 publications

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“…Alternatively, drugs can be added in the culture medium to stimulated myotube formation (e.g. HGF, FGF, IGF-1, DEX)[ 23 ] or muscle contraction (e.g. caffeine) [ 74 ].…”

Section: Discussionmentioning

confidence: 99%

Satellite cells delivered in their niche efficiently generate functional myotubes in three-dimensional cell culture

et al. 2018

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Biophysical/biochemical cues from the environment contribute to regulation of the regenerative capacity of resident skeletal muscle stem cells called satellites cells. This can be observed in vitro, where muscle cell behaviour is influenced by the particular culture substrates and whether culture is performed in a 2D or 3D environment, with changes including morphology, nuclear shape and cytoskeletal organization. To create a 3D skeletal muscle model we compared collagen I, Fibrin or PEG-Fibrinogen with different sources of murine and human myogenic cells. To generate tension in the 3D scaffold, biomaterials were polymerised between two flexible silicone posts to mimic tendons. This 3D culture system has multiple advantages including being simple, fast to set up and inexpensive, so providing an accessible tool to investigate myogenesis in a 3D environment. Immortalised human and murine myoblast lines, and primary murine satellite cells showed varying degrees of myogenic differentiation when cultured in these biomaterials, with C2 myoblasts in particular forming large multinucleated myotubes in collagen I or Fibrin. However, murine satellite cells retained in their niche on a muscle fibre and embedded in 3D collagen I or Fibrin gels generated aligned, multinucleated and contractile myotubes.

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“…Alternatively, drugs can be added in the culture medium to stimulated myotube formation (e.g. HGF, FGF, IGF-1, DEX)[ 23 ] or muscle contraction (e.g. caffeine) [ 74 ].…”

Section: Discussionmentioning

confidence: 99%

Satellite cells delivered in their niche efficiently generate functional myotubes in three-dimensional cell culture

et al. 2018

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“…Several growth factors have been delivered intramuscularly, systemically, or via biomaterial carriers to aid muscle healing. These include among others, hepatocyte growth factor (HGF), insulin‐like growth factor (IGF), vascular endothelial growth factor (VEGF), and fibroblast growth factor . HGF is known to stimulate the activation of quiescent SCs, promoting their proliferation and migration while inhibiting their premature differentiation .…”

Section: Advances In Treatment Of Local Muscle Injuriesmentioning

confidence: 99%

Cell therapy to improve regeneration of skeletal muscle injuries

Qazi

Duda

Ort

et al. 2019

J cachexia sarcopenia muscle

106

128

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Diseases that jeopardize the musculoskeletal system and cause chronic impairment are prevalent throughout the Western world. In Germany alone, ~1.8 million patients suffer from these diseases annually, and medical expenses have been reported to reach 34.2bn Euros. Although musculoskeletal disorders are seldom fatal, they compromise quality of life and diminish functional capacity. For example, musculoskeletal disorders incur an annual loss of over 0.8 million workforce years to the German economy. Among these diseases, traumatic skeletal muscle injuries are especially problematic because they can occur owing to a variety of causes and are very challenging to treat. In contrast to chronic muscle diseases such as dystrophy, sarcopenia, or cachexia, traumatic muscle injuries inflict damage to localized muscle groups. Although minor muscle trauma heals without severe consequences, no reliable clinical strategy exists to prevent excessive fibrosis or fatty degeneration, both of which occur after severe traumatic injury and contribute to muscle degeneration and dysfunction. Of the many proposed strategies, cell‐based approaches have shown the most promising results in numerous pre‐clinical studies and have demonstrated success in the handful of clinical trials performed so far. A number of myogenic and non‐myogenic cell types benefit muscle healing, either by directly participating in new tissue formation or by stimulating the endogenous processes of muscle repair. These cell types operate via distinct modes of action, and they demonstrate varying levels of feasibility for muscle regeneration depending, to an extent, on the muscle injury model used. While in some models the injury naturally resolves over time, other models have been developed to recapitulate the peculiarities of real‐life injuries and therefore mimic the structural and functional impairment observed in humans. Existing limitations of cell therapy approaches include issues related to autologous harvesting, expansion and sorting protocols, optimal dosage, and viability after transplantation. Several clinical trials have been performed to treat skeletal muscle injuries using myogenic progenitor cells or multipotent stromal cells, with promising outcomes. Recent improvements in our understanding of cell behaviour and the mechanistic basis for their modes of action have led to a new paradigm in cell therapies where physical, chemical, and signalling cues presented through biomaterials can instruct cells and enhance their regenerative capacity. Altogether, these studies and experiences provide a positive outlook on future opportunities towards innovative cell‐based solutions for treating traumatic muscle injuries—a so far unmet clinical need.

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“…By using various growth factors, including hepatocyte growth factor, fibroblast growth factors, and insulin-like growth factor, properties of newly formed skeletal muscle tissue can be similar to that of native muscle. 7 , 8 , 9 , 10 Regardless of the regenerating potential of skeletal muscle, however, scar formation is unavoidable. 11 Scar, or fibrosis, is the abnormal accumulation of extracellular matrix (ECM).…”

Section: Introductionmentioning

confidence: 99%

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

Sun

Wang

et al. 2018

Molecular Therapy - Nucleic Acids

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Fibrosis is common after skeletal muscle injury, undermining tissue regeneration and function. The mechanism underlying skeletal muscle fibrosis remains unveiled. Transforming growth factor-β/Smad signaling pathway is supposed to play a pivotal role. However, how microRNAs interact with transforming growth factor-β/Smad-related muscle fibrosis remains unclear. We showed that microRNA (miR)-24-3p and miR-122-5p declined in skeletal muscle fibrosis, which was a consequence of transforming growth factor-β. Upregulating Smad4 suppressed two microRNAs, whereas inhibiting Smad4 elevated microRNAs. Luciferase reporter assay and chromatin immunoprecipitation confirmed that Smad4 directly inhibited two microRNAs. On the other hand, overexpression of these two miRs retarded fibrotic process. We further identified that Smad2 was a direct target of miR-24-3p, whereas miR-122-5p targeted transforming growth factor-β receptor-II. Both targets were important participants in transforming growth factor-β/Smad signaling. Taken together, a positive feedback loop in transforming growth factor-β/Smad4 signaling pathway in skeletal muscle fibrosis was identified. Transforming growth factor-β/Smad axis could be downregulated by microRNAs. This effect, however, was suppressed by Smad4, the downstream of transforming growth factor-β.

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Growth Factors for Skeletal Muscle Tissue Engineering

Cited by 60 publications

References 57 publications

Satellite cells delivered in their niche efficiently generate functional myotubes in three-dimensional cell culture

Satellite cells delivered in their niche efficiently generate functional myotubes in three-dimensional cell culture

Cell therapy to improve regeneration of skeletal muscle injuries

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

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