Transforming growth factor-?2 is elevated in skeletal muscle disorders

Murakami, Nobuyuki; McLennan, Ian S.; Nonaka, Ikuya; Koishi, Kyoko; Baker, Christina M.; Hammond-Tooke, Graeme

doi:10.1002/(sici)1097-4598(199907)22:7<889::aid-mus12>3.0.co;2-b

Cited by 57 publications

(33 citation statements)

References 33 publications

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“…In muscles of patients with myotubular myopathy, low levels of CTGF were observed at the center of myofibers. Murakami et al reported the immunolocalization of TGF-beta2 at the center of myofibers in patients with myotubular myopathy [46]. This suggests that growth factors have a role other than that in the regeneration of muscle fibers, but this role has yet to be determined.…”

Section: Discussionmentioning

confidence: 99%

Connective tissue growth factor is overexpressed in muscles of human muscular dystrophy

Sun

Haginoya

et al. 2008

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 99%

Connective tissue growth factor is overexpressed in muscles of human muscular dystrophy

Sun

Haginoya

et al. 2008

Journal of the Neurological Sciences

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“…Another cytokine that may be of importance in muscle regeneration in the absence of TNF-␣ is transforming growth factor-beta (TGF-␤) (Derynck and Choy 1998). In particular, TGF-␤ is a modulator of myoblast differentiation and fusion and in remodeling of the extracellular matrix (Murakami et al 1999). TGF-␤ also attenuates the inflammatory response and inhibits the activity andրor production of a number of cytokines, including TNF-␣, LT-␣, and IL-1 (Derynck and Choy 1998).…”

Section: Cytokine Interactionsmentioning

confidence: 99%

“…TGF-␤ also attenuates the inflammatory response and inhibits the activity andրor production of a number of cytokines, including TNF-␣, LT-␣, and IL-1 (Derynck and Choy 1998). Like TNF-␣, TGF-␤ is also elevated in skeletal muscle disorders (Murakami et al 1999). However, because the muscles of TGF-␤(-ր-) mice appear normal (McLennan et al 2000), this indicates that other genes are capable of substituting for the missing TGF-␤ in vivo.…”

Section: Cytokine Interactionsmentioning

confidence: 99%

The Role of Tumor Necrosis Factor-alpha (TNF-α) in Skeletal Muscle Regeneration

Collins

Grounds²

2001

J Histochem Cytochem.

147

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The role of tumor necrosis factor-alpha (TNF-α), an important mediator of the inflammatory response after injury, was investigated in regenerating skeletal muscle. The pattern of expression of TNF-α during muscle regeneration was examined by immunohistochemistry in tissue sections of crush-injured or transplanted muscle autografts and in primary cultures of adult skeletal muscle. TNF-α was highly expressed in injured myofibers, inflammatory cells, endothelial cells, fibroblasts, and mast cells. Myoblasts and myotubes also expressed TNF-α in primary muscle cultures and tissue sections. The essential role of TNF-α and its homologue lymphotoxin-alpha (LT-α) during muscle regeneration was assessed by basic histology in TNF-α(–) and TNF-α(-/-)/LT-α(-/-) mice. No difference was apparent in the onset or pattern of muscle regeneration (i.e., inflammatory response, activation and fusion of myoblasts) between the two strains of null mice or between nulls and normal control mice. However, both strains of null mice appeared more prone to bystander damage of host muscle and regeneration distant from the site of injury/transplantation. Although expression of TNF-α may play an important role in muscle regeneration, the studies in the null mice show that redundancy within the cytokine system (or some other response) can effectively compensate for the absence of TNF-α in vivo. (J Histochem Cytochem 49:989–1001, 2001)

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“…In myopathies such as Duchenne muscular dystrophy (DMD), the regeneration process is compromised, and muscle tissue is replaced by dysfunctional scar (fibrotic) tissue. Levels of TGF-b1 and TGF-b2 are elevated in muscular dystrophies and have been shown to cause fibrosis in dystrophic muscles (Bernasconi et al, 1995;Bernasconi et al, 1999;Murakami et al, 1999;Zhu et al, 2007). Interestingly, inhibition of TGF-b signaling not only prevents fibrosis, but also improves regeneration in mdx mutants that are widely studied as a mouse model for DMD (Lefaucheur and Sébille, 1995;Cohn et al, 2007), indicating that regulation of fibrosis presents a key step in the pathology of DMD.…”

Section: Introductionmentioning

confidence: 99%

Sharp-1 regulates TGF-β signaling and skeletal muscle regeneration

Acharjee

Chung

Gopinadhan

et al. 2013

Journal of Cell Science

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Sharp-1 is a basic helix-loop-helix (bHLH) transcriptional repressor that is involved in a number of cellular processes. Our previous studies have demonstrated that Sharp-1 is a negative regulator of skeletal myogenesis and it blocks differentiation of muscle precursor cells by modulating the activity of MyoD. In order to understand its role in pre-and post-natal myogenesis, we assessed skeletal muscle development and freeze-injury-induced regeneration in Sharp-1-deficient mice. We show that embryonic skeletal muscle development is not impaired in the absence of Sharp-1; however, post-natally, the regenerative capacity is compromised. Although the initial phases of injury-induced regeneration proceed normally in Sharp-1 2/2 mice, during late stages, the mutant muscle exhibits necrotic fibers, calcium deposits and fibrosis. TGF-b expression, as well as levels of phosphorylated Smad2 and Smad3, are sustained in the mutant tissue and treatment with decorin, which blocks TGF-b signaling, improves the histopathology of Sharp-1 2/2 injured muscles. In vitro, Sharp-1 associates with Smad3, and its overexpression inhibits TGF-b-and Smad3-mediated expression of extracellular matrix genes in myofibroblasts. These results demonstrate that Sharp-1 regulates muscle regenerative capacity, at least in part, by modulation of TGF-b signaling.

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Transforming growth factor-?2 is elevated in skeletal muscle disorders

Cited by 57 publications

References 33 publications

Connective tissue growth factor is overexpressed in muscles of human muscular dystrophy

Connective tissue growth factor is overexpressed in muscles of human muscular dystrophy

The Role of Tumor Necrosis Factor-alpha (TNF-α) in Skeletal Muscle Regeneration

Sharp-1 regulates TGF-β signaling and skeletal muscle regeneration

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