scholarly journals Stra13 regulates satellite cell activation by antagonizing Notch signaling

2007 ◽  
Vol 177 (4) ◽  
pp. 647-657 ◽  
Author(s):  
Hong Sun ◽  
Li Li ◽  
Cécile Vercherat ◽  
Neriman Tuba Gulbagci ◽  
Sujata Acharjee ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Cell Activation ◽  
Cellular Proliferation ◽  
Myogenic Differentiation ◽  
Critical Role ◽  
Skeletal Muscle Regeneration ◽  
Notch Activity ◽  
Satellite Cell Activation

Satellite cells play a critical role in skeletal muscle regeneration in response to injury. Notch signaling is vital for satellite cell activation and myogenic precursor cell expansion but inhibits myogenic differentiation. Thus, precise spatial and temporal regulation of Notch activity is necessary for efficient muscle regeneration. We report that the basic helix-loop-helix transcription factor Stra13 modulates Notch signaling in regenerating muscle. Upon injury, Stra13−/− mice exhibit increased cellular proliferation, elevated Notch signaling, a striking regeneration defect characterized by degenerated myotubes, increased mononuclear cells, and fibrosis. Stra13−/− primary myoblasts also exhibit enhanced Notch activity, increased proliferation, and defective differentiation. Inhibition of Notch signaling ex vivo and in vivo ameliorates the phenotype of Stra13−/− mutants. We demonstrate in vitro that Stra13 antagonizes Notch activity and reverses the Notch-imposed inhibition of myogenesis. Thus, Stra13 plays an important role in postnatal myogenesis by attenuating Notch signaling to reduce myoblast proliferation and promote myogenic differentiation.

Skeletal muscle regeneration is delayed by reduction in Xin expression: consequence of impaired satellite cell activation?

2012 ◽  
Vol 302 (1) ◽  
pp. C220-C227 ◽  
Author(s):  
Aliyah A. Nissar ◽  
Bart Zemanek ◽  
Rita Labatia ◽  
Daniel J. Atkinson ◽  
Peter F. M. van der Ven ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Tibialis Anterior ◽  
Cell Activation ◽  
Striated Muscle ◽  
Critical Role ◽  
Skeletal Muscle Regeneration ◽  
Actin Binding ◽  
Cell Cycle Reentry ◽  
Satellite Cell Activation

Xin is a striated muscle-specific actin-binding protein whose mRNA expression has been observed in damaged skeletal muscle. Here we demonstrate increased Xin protein expression early postinjury (≤12 h) and localization primarily to the periphery of damaged myofibers. At 1 day postinjury, Xin is colocalized with MyoD, confirming expression in activated satellite cells (SCs). By 5 days postinjury, Xin is evident in newly regenerated myofibers, with a return to preinjury levels by 14 days of regeneration. To determine whether the increased Xin expression is functionally relevant, tibialis anterior muscles of wild-type mice were infected with Xin-short hairpin RNA (shRNA) adenovirus, whereas the contralateral tibialis anterior received control adenovirus (Control). Four days postinfection, muscles were harvested or injured with cardiotoxin and collected at 3, 5, or 14 days thereafter. When compared with Control, Xin-shRNA infection attenuated muscle regeneration as demonstrated by Myh3 expression and fiber areas. Given the colocalization of Xin and MyoD, we isolated single myofibers from infected muscles to investigate the effect of silencing Xin on SC function. Relative to Control, SC activation, but not proliferation, was significantly impaired in Xin-shRNA-infected muscles. To determine whether Xin affects the G0-G1 transition, cell cycle reentry was assessed on infected C2C12 myoblasts using a methylcellulose assay. No difference in reentry was noted between groups, suggesting that Xin contributes to SC activation by means other than affecting G0-G1 transition. Together these data demonstrate a critical role for Xin in SC activation and reduction in Xin expression results in attenuated skeletal muscle repair.

scholarly journals Lack of robust satellite cell activation and muscle regeneration during the progression of Pompe disease

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Gerben J. Schaaf ◽  
Tom JM van Gestel ◽  
Esther Brusse ◽  
Robert M. Verdijk ◽  
Irenaeus FM de Coo ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Pompe Disease ◽  
Muscle Regeneration ◽  
Cell Activation ◽  
Satellite Cell Activation

scholarly journals Metformin Delays Satellite Cell Activation and Maintains Quiescence

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Theodora Pavlidou ◽  
Milica Marinkovic ◽  
Marco Rosina ◽  
Claudia Fuoco ◽  
Simone Vumbaca ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Muscle Tissue ◽  
Satellite Cells ◽  
Cell Activation ◽  
Myogenic Differentiation ◽  
Metabolic State ◽  
Cell Pool ◽  
Age Related ◽  
Satellite Cell Activation

The regeneration of the muscle tissue relies on the capacity of the satellite stem cell (SC) population to exit quiescence, divide asymmetrically, proliferate, and differentiate. In age-related muscle atrophy (sarcopenia) and several dystrophies, regeneration cannot compensate for the loss of muscle tissue. These disorders are associated with the depletion of the satellite cell pool or with the loss of satellite cell functionality. Recently, the establishment and maintenance of quiescence in satellite cells have been linked to their metabolic state. In this work, we aimed to modulate metabolism in order to preserve the satellite cell pool. We made use of metformin, a calorie restriction mimicking drug, to ask whether metformin has an effect on quiescence, proliferation, and differentiation of satellite cells. We report that satellite cells, when treated with metformin in vitro, ex vivo, or in vivo, delay activation, Pax7 downregulation, and terminal myogenic differentiation. We correlate the metformin-induced delay in satellite cell activation with the inhibition of the ribosome protein RPS6, one of the downstream effectors of the mTOR pathway. Moreover, in vivo administration of metformin induces a belated regeneration of cardiotoxin- (CTX-) damaged skeletal muscle. Interestingly, satellite cells treated with metformin immediately after isolation are smaller in size and exhibit reduced pyronin Y levels, which suggests that metformin-treated satellite cells are transcriptionally less active. Thus, our study suggests that metformin delays satellite cell activation and differentiation by favoring a quiescent, low metabolic state.

scholarly journals Premature satellite cell activation before injury accelerates myogenesis and disrupts neuromuscular junction maturation in regenerating muscle

2020 ◽  
Vol 319 (1) ◽  
pp. C116-C128
Author(s):  
Nasibeh Daneshvar ◽  
Ryuichi Tatsumi ◽  
Jason Peeler ◽  
Judy E. Anderson
Keyword(s):  
Axon Guidance ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Cell Activation ◽  
Neuromuscular Junctions ◽  
Muscle Repair ◽  
No Donor ◽  
Satellite Cell Activation ◽  
Models Of Injury ◽  
Terminal Schwann Cells

Satellite cell (SC) activation, mediated by nitric oxide (NO), is essential to myogenic repair, whereas myotube function requires innervation. Semaphorin (Sema) 3A, a neuro-chemorepellent, is thought to regulate axon guidance to neuromuscular junctions (NMJs) during myotube differentiation. We tested whether “premature” SC activation (SC activation before injury) by a NO donor (isosorbide dinitrate) would disrupt early myogenesis and/or NMJs. Adult muscle was examined during regeneration in two models of injury: myotoxic cardiotoxin (CTX) and traumatic crush (CR) ( n = 4–5/group). Premature SC activation was confirmed by increased DNA synthesis by SCs immediately in pretreated mice after CTX injury. Myotubes grew faster after CTX than after CR; growth was accelerated by pretreatment. NMJ maturation, classified by silver histochemistry (neurites) and acetylcholinesterase (AchE), and α-bungarotoxin staining (Ach receptors, AchRs) were delayed by pretreatment, consistent with a day 6 rise in the denervation marker γ-AchR. With pretreatment, S100B from terminal Schwann cells (TSCs) increased 10- to 20-fold at days 0 and 10 after CTX and doubled 6 days after CR. Premature SC activation disrupted motoneuritogenesis 8–10 days post-CTX, as pretreatment reduced colocalization of pre- and postsynaptic NMJ features and increased Sema3A-65. Premature SC activation before injury both accelerated myogenic repair and disrupted NMJ remodeling and maturation, possibly by reducing Sema3A neuro-repulsion and altering S100B. This interpretation extends the model of Sema3A-mediated motoneuritogenesis during muscle regeneration. Manipulating the timing and type of Sema3A by brief NO effects on SCs suggests an important role for TSCs and Sema3A-65 processing in axon guidance and NMJ restoration during muscle repair.

scholarly journals HDAC 4 promotes P ax7‐dependent satellite cell activation and muscle regeneration

EMBO Reports ◽  
2014 ◽  
Vol 15 (11) ◽  
pp. 1175-1183 ◽  
Author(s):  
Moon‐Chang Choi ◽  
Soyoung Ryu ◽  
Rui Hao ◽  
Bin Wang ◽  
Meghan Kapur ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Muscle Regeneration ◽  
Cell Activation ◽  
Satellite Cell Activation

scholarly journals miR-378 attenuates muscle regeneration by delaying satellite cell activation and differentiation in mice

2016 ◽  
Vol 48 (9) ◽  
pp. 833-839 ◽  
Author(s):  
Ping Zeng ◽  
Wanhong Han ◽  
Changyin Li ◽  
Hu Li ◽  
Dahai Zhu ◽  
...  
Keyword(s):  
Satellite Cell ◽  
Muscle Regeneration ◽  
Cell Activation ◽  
Satellite Cell Activation
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