Skeletal muscle cells express the profibrotic cytokine connective tissue growth factor (CTGF/CCN2), which induces their dedifferentiation

@article{Vial2008SkeletalMC,
  title={Skeletal muscle cells express the profibrotic cytokine connective tissue growth factor (CTGF/CCN2), which induces their dedifferentiation},
  author={Cecilia Vial and Lidia M. Z{\'u}{\~n}iga and Claudio Cabello-Verrugio and Pablo M. Ca{\~n}{\'o}n and Ricardo Fadi{\'c} and Enrique Brandan},
  journal={Journal of Cellular Physiology},
  year={2008},
  volume={215}
}
Fibrotic disorders are typified by excessive connective tissue and extracellular matrix (ECM) deposition that precludes normal healing processes of different tissues. Connective tissue growth factor (CTGF) seems to be involved in the fibrotic response. Several muscular dystrophies are characterized by a progressive weakness and wasting of the musculature, and by extensive fibrosis. However, the exact role of CTGF in skeletal muscle is unknown. Here we show that myoblasts and myotubes are able… Expand
Constitutively activated dystrophic muscle fibroblasts show a paradoxical response to TGF-β and CTGF/CCN2
TLDR
Regardless of the absence of degenerative myofibers, adult mdx diaphragm fibroblasts show increased levels of FN and condroitin/dermatan sulfate PGs synthesis, hypothesize that a pathological environment is able to reprogram fibro Blasts into an activated phenotype which can be maintained through generations. Expand
The pro-fibrotic connective tissue growth factor (CTGF/CCN2) correlates with the number of necrotic-regenerative foci in dystrophic muscle
TLDR
CCN2 appears to be involved in the fibrotic response as well as in the inflammatory response in the dystrophic skeletal muscle. Expand
Role of hypoxia in skeletal muscle fibrosis: Synergism between hypoxia and TGF-β signaling upregulates CCN2/CTGF expression specifically in muscle fibers.
TLDR
In vivo experiments using pharmacological stabilization of HIF-1α or hypoxia-induced via hindlimb ischemia together with intramuscular injections of TGF-β1, and increased CCN2 expression are found suggest that hypoxic signaling together with T GF-β signaling, which are both characteristics of a fibrotic skeletal muscle environment, induce the expression of CCN 2 in skeletal muscle fibers and myotubes. Expand
Denervation-induced skeletal muscle fibrosis is mediated by CTGF/CCN2 independently of TGF-β.
TLDR
The results suggest that in this model CTGF/CCN2 is not up-regulated by canonical TGF-β signaling early after denervation and that other factors are likely involved in the early fibrotic response following skeletal muscle denervation. Expand
SMAD3 and SP1/SP3 Transcription Factors Collaborate to Regulate Connective Tissue Growth Factor Gene Expression in Myoblasts in Response to Transforming Growth Factor β
TLDR
It is suggested that additional transcription factor binding sites (TFBS) present in the 5' UTR of the CTGF gene are important for this expression and that SP1/SP3 factors are involved in TGF‐β‐mediated CTGF expression. Expand
Transforming growth factor type-β inhibits Mas receptor expression in fibroblasts but not in myoblasts or differentiated myotubes; Relevance to fibrosis associated to muscular dystrophies.
TLDR
It is suggested that reduction of Mas receptor in fibroblasts, by TGF-β, could increase the fibrotic phenotype observed in dystrophic skeletal muscle decreasing the beneficial effect of Ang-(1-7). Expand
Genetic manipulation of CCN2/CTGF unveils cell‐specific ECM‐remodeling effects in injured skeletal muscle
TLDR
The results show that the myofibers are critical mediators of the deleterious effects associated with CTGF in MD and acutely injured skeletal muscle. Expand
CTGF/CCN‐2 over‐expression can directly induce features of skeletal muscle dystrophy
Muscular dystrophies are diseases characterized by muscle weakness together with cycles of degeneration and regeneration of muscle fibres, resulting in a progressive decrease of muscle mass,Expand
Role of CTGF and TNF on fibrosis in muscular dystrophy
TLDR
The increased expression of the soluble TNF Receptor I by electrotransfer (ET) in the tibialis anterior muscle attenuates inflammation, damage and fibrosis in the skeletal muscle of the mdx mice and proposes that ET could be used as an efficient anti-TNF therapy for treating muscle dystrophies. Expand
Decorin Interacts with Connective Tissue Growth Factor (CTGF)/CCN2 by LRR12 Inhibiting Its Biological Activity*
TLDR
The results suggest that decorin interacts with CTGF and regulates its biological activity, and shows that CTGF specifically induced the synthesis of decorin, suggesting a mechanism of autoregulation. Expand
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TLDR
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TLDR
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