MyoD expression restores defective myogenic differentiation of human mesoangioblasts from inclusion-body myositis muscle

Morosetti, Roberta; Mirabella, Massimiliano; Gliubizzi, Carla; Broccolini, Aldobrando; Angelis, Luciana De; Tagliafico, Enrico; Sampaolesi, Maurilio; Gidaro, T.; Papacci, Manuela; Roncaglia, Enrica; Rutella, Sergio; Ferrari, Stefano; Tonali, P.; Ricci, Enzo; Cossu, Giulio

doi:10.1073/pnas.0603386103

Cited by 70 publications

(81 citation statements)

References 29 publications

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“…It was observed that mesoangioblasts from the IBM patients could not differentiate into myofibers when cultured in vitro or xenotransplanted into injured mouse muscles. Interestingly, this defect can be rescued by either transient overexpressing of MyoD or knockdown of a MyoD inhibitor protein, bHLH-B3, which suggests that the myogenic program of mesoangioblasts is MyoD-dependent (352). Several investigations demonstrated that factors involved in normal muscle regeneration also facilitate mesoangioblastbased muscle regeneration.…”

Section: Mesoangioblastsmentioning

confidence: 97%

“…In addition, mesoangioblasts can release immunosuppressive and tolerogenic molecules, which supposedly help mesoangioblasts incorporate into allogeneic dystrophic hosts (211). The myogenic potential of mesoangioblasts isolated from human patient biopsies suffering from dermatomyositis (DM), polymyositis (PM) and inclusion-body myositis (IBM) were compared (352). It was observed that mesoangioblasts from the IBM patients could not differentiate into myofibers when cultured in vitro or xenotransplanted into injured mouse muscles.…”

Section: Mesoangioblastsmentioning

confidence: 99%

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Satellite Cells and the Muscle Stem Cell Niche

Yin

Price

Rudnicki

2013

Physiological Reviews

1,759

1,808

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LYin H, Price F, Rudnicki MA. Satellite Cells and the Muscle Stem Cell Niche. Physiol Rev 93: 23-67, 2013; doi:10.1152/physrev.00043.2011.-Adult skeletal muscle in mammals is a stable tissue under normal circumstances but has remarkable ability to repair after injury. Skeletal muscle regeneration is a highly orchestrated process involving the activation of various cellular and molecular responses. As skeletal muscle stem cells, satellite cells play an indispensible role in this process. The self-renewing proliferation of satellite cells not only maintains the stem cell population but also provides numerous myogenic cells, which proliferate, differentiate, fuse, and lead to new myofiber formation and reconstitution of a functional contractile apparatus. The complex behavior of satellite cells during skeletal muscle regeneration is tightly regulated through the dynamic interplay between intrinsic factors within satellite cells and extrinsic factors constituting the muscle stem cell niche/microenvironment. For the last half century, the advance of molecular biology, cell biology, and genetics has greatly improved our understanding of skeletal muscle biology. Here, we review some recent advances, with focuses on functions of satellite cells and their niche during the process of skeletal muscle regeneration.

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Section: Mesoangioblastsmentioning

confidence: 97%

Section: Mesoangioblastsmentioning

confidence: 99%

Satellite Cells and the Muscle Stem Cell Niche

Yin

Price

Rudnicki

2013

Physiological Reviews

1,759

1,808

View full text Add to dashboard Cite

show abstract

“…3 and 4) is reminiscent of loss of differentiated myoepithelial cells in some salivary and breast cancers. 31,32,64 Since TGFb1 function has been shown to promote the expression of smooth muscle and contractile proteins, such as SM aactin, [65][66][67] and is implicated in the tumor-suppressive activities of myoepithelial cells, 64 we tested TGFb1 for its ability to rescue myoepithelial differentiation in the disrupted SMG organ explants grown at 19.66 kPa. Both AQP5 and SM a-actin expression was partially rescued with the addition of 2-5 ng/mL TGFb1 to the media (Fig.…”

Section: Rescuing the 1966 Kpa Phenotypementioning

confidence: 99%

Biocompatible Tissue Scaffold Compliance Promotes Salivary Gland Morphogenesis and Differentiation

Peters

Naim

Nelson

et al. 2014

Tissue Engineering Part A

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Substrate compliance is reported to alter cell phenotype, but little is known about the effects of compliance on cell development within the context of a complex tissue. In this study, we used 0.48 and 19.66 kPa polyacrylamide gels to test the effects of the substrate modulus on submandibular salivary gland development in culture and found a significant decrease in branching morphogenesis in explants grown on the stiff 19.66 kPa gels relative to those grown on the more physiologically compliant 0.48 kPa gels. While proliferation and apoptosis were not affected by the substrate modulus, tissue architecture and epithelial acinar cell differentiation were profoundly perturbed by aberrant, high stiffness. The glands cultured on 0.48 kPa gels were similar to developing glands in morphology and expression of the differentiation markers smooth muscle alpha-actin (SM a-actin) in developing myoepithelial cells and aquaporin 5 (AQP5) in proacinar cells. At 19.66 kPa, however, tissue morphology and the expression and distribution of SM a-actin and AQP5 were disrupted. Significantly, aberrant gland development at 19.66 kPa could be rescued by both mechanical and chemical stimuli. Transfer of glands from 19.66 to 0.48 kPa gels resulted in substantial recovery of acinar structure and differentiation, and addition of exogenous transforming growth factor beta 1 at 19.66 kPa resulted in a partial rescue of morphology and differentiation within the proacinar buds. These results indicate that environmental compliance is critical for organogenesis, and suggest that both mechanical and chemical stimuli can be exploited to promote organ development in the contexts of tissue engineering and organ regeneration.

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“…Intriguingly, however, myogenic differentiation is augmented at early stages in Sharp-1 mutant tissue, as seen by the increased number of eMHC + cells. This probably occurs because Sharp-1 is a potent inhibitor of MyoD activity and myogenic differentiation (Azmi et al, 2004;Morosetti et al, 2006;Ling et al, 2012;Wang et al, 2013). Its absence therefore would presumably result in increased MyoD activity that could counter the inhibitory effects of TGF-b at early stages in Sharp-1 2/2 mutants.…”

Section: Discussionmentioning

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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MyoD expression restores defective myogenic differentiation of human mesoangioblasts from inclusion-body myositis muscle

Cited by 70 publications

References 29 publications

Satellite Cells and the Muscle Stem Cell Niche

Satellite Cells and the Muscle Stem Cell Niche

Biocompatible Tissue Scaffold Compliance Promotes Salivary Gland Morphogenesis and Differentiation

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

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