A Critical Requirement for Notch Signaling in Maintenance of the Quiescent Skeletal Muscle Stem Cell State

Mourikis, Philippos; Sambasivan, Ramkumar; Castel, David; Rocheteau, Pierre; Bizzarro, Valentina; Tajbakhsh, Shahragim

doi:10.1002/stem.775

Cited by 415 publications

(475 citation statements)

References 40 publications

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“…Inhibition of the Notch signaling in satellite cells, as well as the deficiency of Ten‐4 as shown in this study, forces to exit the quiescent state 13, 14, 15. Brohl et al reported that the Ten‐4 expression level was significantly reduced in the double knockout mice of RBP‐J and MyoD, where Notch signaling was deactivated.…”

Section: Discussionsupporting

confidence: 54%

Muscle Satellite Cell Protein Teneurin-4 Regulates Differentiation During Muscle Regeneration

et al. 2015

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Satellite cells are maintained in an undifferentiated quiescent state, but during muscle regeneration they acquire an activated stage, and initiate to proliferate and differentiate as myoblasts. The transmembrane protein teneurin‐4 (Ten‐4) is specifically expressed in the quiescent satellite cells; however, its cellular and molecular functions remain unknown. We therefore aimed to elucidate the function of Ten‐4 in muscle satellite cells. In the tibialis anterior (TA) muscle of Ten‐4‐deficient mice, the number and the size of myofibers, as well as the population of satellite cells, were reduced with/without induction of muscle regeneration. Furthermore, we found an accelerated activation of satellite cells in the regenerated Ten‐4‐deficient TA muscle. The cell culture analysis using primary satellite cells showed that Ten‐4 suppressed the progression of myogenic differentiation. Together, our findings revealed that Ten‐4 functions as a crucial player in maintaining the quiescence of muscle satellite cells. Stem Cells 2015;33:3017–3027

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Section: Discussionsupporting

confidence: 54%

Muscle Satellite Cell Protein Teneurin-4 Regulates Differentiation During Muscle Regeneration

et al. 2015

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“…However, the effect of depletion of CD9P-1 is unlikely to be a consequence of altered Notch signalling as we observed no significant change in the expression of Notch targets, hes-1 and hey-1 ( Supplementary Fig. S4g), that have been demonstrated to be under the control of Notch in adult myogenic progenitors 44 . The precise mechanisms through which CD9P-1 regulates muscle cells fusion will require further investigations.…”

Section: Discussionmentioning

confidence: 67%

Normal muscle regeneration requires tight control of muscle cell fusion by tetraspanins CD9 and CD81

et al. 2013

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Skeletal muscle regeneration after injury follows a remarkable sequence of synchronized events. However, the mechanisms regulating the typical organization of the regenerating muscle at different stages remain largely unknown. Here we show that muscle regeneration in mice lacking either CD9 or CD81 is abnormal and characterized by the formation of discrete giant dystrophic myofibres, which form more quickly in the absence of both tetraspanins. We also show that, in myoblasts, these two tetraspanins associate with the immunoglobulin domain molecule CD9P-1 (EWI-F/FPRP), and that grafting of CD9P-1-depleted myoblasts in regenerating muscles also leads to abnormal regeneration. In vitro myotubes lacking CD9P-1 or both CD9 and CD81 fuse with a higher frequency than normal myotubes. Our study unveils a mechanism preventing inappropriate fusion of myotubes that has an important role in the restitution of normal muscle architecture during muscle regeneration.

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“…[6][7][8][9][10][11] The expression of Hes1 induced by Notch can be detected more than embryo neural stem cells, intestinal crypt progenitor cells, pancreatic stem cells, bone marrow mesenchymal progenitors and quiescent skeletal muscle stem cells. 9,10,[68][69][70][71] Treatment with g-secretase inhibitor (GSI) results in the suppression of Hes1 and the differentiating state of those stem cells, indicating the role of the Notch pathway in Hes1 expression, as well as the essential status of the Notch-Hes1 pathway in facilitating cell fate decisions and regulating differentiation during development.…”

Section: Canonical Notch Signaling Pathwaymentioning

confidence: 99%

Hes1: a key role in stemness, metastasis and multidrug resistance

Liu¹,

Dai²,

Du³

2015

Cancer Biology & Therapy

152

116

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A Critical Requirement for Notch Signaling in Maintenance of the Quiescent Skeletal Muscle Stem Cell State

Abstract: Notch signaling plays a key role in virtually all tissues and organs in metazoans; however, limited examples are available for the regulatory role of this pathway in adult quiescent stem cells. We performed a temporal and onto-

Cited by 415 publications

References 40 publications

Muscle Satellite Cell Protein Teneurin-4 Regulates Differentiation During Muscle Regeneration

Muscle Satellite Cell Protein Teneurin-4 Regulates Differentiation During Muscle Regeneration

Normal muscle regeneration requires tight control of muscle cell fusion by tetraspanins CD9 and CD81

Hes1: a key role in stemness, metastasis and multidrug resistance

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