A Twist2-dependent progenitor cell contributes to adult skeletal muscle

Liu, Ning; Garry, Glynnis A.; Li, Stephen; Bezprozvannaya, Svetlana; Sánchez-Ortiz, Efrain; Chen, Beibei; Shelton, John M.; Jaichander, Priscilla; Bassel‐Duby, Rhonda; Olson, Eric N.

doi:10.1038/ncb3477

Cited by 124 publications

(177 citation statements)

References 54 publications

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“…9). Additionally, some genes involved in the smooth muscle maturation and skeletal myogenesis, as reported in previous studies (31)(32)(33)(34)(35)(36), were also found to be differentially expressed in CK14-Cre;Shh fl/fl mutant mice ( Fig. 9).…”

Section: Discussionsupporting

confidence: 78%

Loss of sonic hedgehog gene leads to muscle development disorder and megaesophagus in mice

et al. 2018

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Sonic hedgehog ( Shh) is crucial for organogenesis in the foregut. This study investigated the function of Shh at the late-gestational stage; during which, the esophagus continues to differentiate. We established cytokeratin 14 ( CK14)-Cre;Shh mice in which the down-regulation of Shh in the epithelium occurred at approximately the same time as esophageal muscle conversion. Hematoxylin and eosin and immunohistochemical staining, with antibodies against keratin 14, Shh, patched 1 (Ptch1), Gli1, proliferating cell nuclear antigen (PCNA), α-smooth muscle actin (αSMA), high-molecular-weight caldesmon (hCD), myogenin, paired box 7 (Pax7), β3-tubulin, and protein gene product 9.5 (PGP9.5), was performed to detect specific tissue dysplasia. Organ culture was conducted in vitro, and total mRNA was extracted to determine the transcriptional dysregulation. The esophagus of CK14-Cre;Shh mice developed into an independent tube with an obvious dilatation at postnatal d 0.5. The number of cell layers and the expression of PCNA were decreased in mutant mice, compared with those in wild-type mice. The expression of hCD declined progressively in the middle, distal, and lower esophageal sphincter levels of the mutant esophagus from embryonic d 17.5, compared with the expression in wild-type littermates. Pax7 accumulation and myogenin reduction in mutant mice indicated that esophageal skeletal-myoblast progression was blocked. RNA sequencing analysis revealed a significant down-regulation of genes involved in proliferation and muscular motivation in CK14-Cre;Shh mice. Thus, loss of Shh at the late-gestational stage leads to megaesophagus with reduced proliferation and a muscle development disorder in mice.-Jia, X., Min, L., Zhu, S., Zhang, S., Huang, X. Loss of sonic hedgehog gene leads to muscle development disorder and megaesophagus in mice.

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Section: Discussionsupporting

confidence: 78%

Loss of sonic hedgehog gene leads to muscle development disorder and megaesophagus in mice

et al. 2018

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“…This may be the precipitating alteration that impacts normal EOM formation, as neural crest cells are crucial for normal EOM development through their expression of retinoic acid [37, 38]. Interestingly, a recent report has shown a Twist1-positive mesenchymal cell population in skeletal muscle which can contribute to the regeneration and maintenance of type II fibers [39]. The potential role of these cells in the EOMs has yet to be determined.…”

Section: Eom Regenerative Cell Populationsmentioning

confidence: 99%

Extraocular Muscle Repair and Regeneration

Verma

Fitzpatrick

McLoon

2017

Curr Ophthalmol Rep

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Purpose of Review The goal of this review is to summarize the unique regenerative milieu within mature mammalian extraocular muscles (EOMs). This will aid in understanding disease propensity for and sparing of EOMs in skeletal muscle diseases as well as the recalcitrance of the EOM to injury. Recent Findings The EOMs continually remodel throughout life and contain an extremely enriched number of myogenic precursor cells that differ in number and functional characteristics from those in limb skeletal muscle. The EOMs also contain a large population of Pitx2-positive myogenic precursor cells that provide the EOMs with many of their unusual biological characteristics, such as myofiber remodeling and skeletal muscle disease sparing. This environment provides for rapid and efficient remodeling and regeneration after various types of injury. In addition, the EOMs show a remarkable ability to respond to perturbations of single muscles with coordinated changes in the other EOMs that move in the same plane. Summary These data will inform Ophthalmologists as they work toward developing new treatments for eye movement disorders, new approaches for repair after nerve or direct EOMs injury, as well as suggest potential explanations for the unusual disease propensity and disease sparing characteristics of human EOM.

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“…In addition to these cell populations, mesenchymal cells that express the transcription factor Twist2 were recently reported to act as myogenic progenitors, however, with selective type IIb fibre-differentiation potential (Liu et al, 2017). PICs (Pw1+ Interstitial Cells) were also reported to engraft efficiently and contribute to myofibre regeneration following intramuscular injection (Mitchell et al, 2010).…”

Section: Cellular Regulators Of Muscle Repair and Their Regenerative mentioning

confidence: 99%

Regulation and phylogeny of skeletal muscle regeneration

Baghdadi

Tajbakhsh

2018

Developmental Biology

158

135

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One of the most fascinating questions in regenerative biology is why some animals can regenerate injured structures while others cannot. Skeletal muscle has a remarkable capacity to regenerate even after repeated traumas, yet limited information is available on muscle repair mechanisms and how they have evolved. For decades, the main focus in the study of muscle regeneration was on muscle stem cells, however, their interaction with their progeny and stromal cells is only starting to emerge, and this is crucial for successful repair and reestablishment of homeostasis after injury. In addition, numerous murine injury models are used to investigate the regeneration process, and some can lead to discrepancies in observed phenotypes. This review addresses these issues and provides an overview of the some of the main regulatory cellular and molecular players involved in skeletal muscle repair.Key words: skeletal muscle, regeneration, stem cells, evolution, quiescence, injury IntroductionThe ability to regenerate tissues and structures is a prevalent feature of metazoans although there is significant variability among species ranging from limited regeneration of a tissue (birds and mammals) to regeneration involving the entire organism (cnidarians, planarians, hydra). The intriguing evolutionary loss of regenerative capacity in more complex organisms highlights the importance of identifying the underlying mechanisms responsible for these diverse regenerative strategies. One of the most studied tissues that contributes to new appendage formation is skeletal muscle, thereby making it a major focus of regeneration studies during evolution. The emergence of new lineage-tracing tools in different animal models has permitted the identification of specific progenitor cell populations and their contribution to tissue repair.Skeletal muscles allow voluntary movement and they play a key role in regulating metabolism and homeostasis in the organism. In mice and humans this tissue represents about 30-40% of the total body mass. This tissue provides an excellent tractable model to study regenerative myogenesis and the relative roles of stem and stromal cells following a single, or repeated rounds of injury. Although muscle regeneration relies mainly on its resident muscle stem (satellite) cells (MuSCs) to effect muscle repair, interactions with neighbouring stromal cells, by direct contact or via the release of soluble factors, is essential to restore proper 3 function. Each step of the myogenic process is regulated by specific regulatory factors including extrinsic cues, yet the nature and source of these signals remain unclear. This review will address these issues and discuss the different experimental models used to investigate the regenerative process. Prenatal and postnatal skeletal muscle developmentIn amniotes, skeletal muscles in the limbs and trunk arise from somites through a series of successive waves that include embryonic and foetal phases of myoblast production (Biressi et al., 2007;Comai and Tajbakhsh, 201...

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A Twist2-dependent progenitor cell contributes to adult skeletal muscle

Cited by 124 publications

References 54 publications

Loss of sonic hedgehog gene leads to muscle development disorder and megaesophagus in mice

Loss of sonic hedgehog gene leads to muscle development disorder and megaesophagus in mice

Extraocular Muscle Repair and Regeneration

Regulation and phylogeny of skeletal muscle regeneration

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