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 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 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.

scholarly journals A Role for Nitric Oxide in Muscle Repair: Nitric Oxide–mediated Activation of Muscle Satellite Cells

2000 ◽  
Vol 11 (5) ◽  
pp. 1859-1874 ◽  
Author(s):  
Judy E. Anderson
Keyword(s):  
Nitric Oxide ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Knockout Mice ◽  
Cell Activation ◽  
Mdx Mice ◽  
Muscle Repair ◽  
Muscle Satellite Cells ◽  
Satellite Cell Activation

Muscle satellite cells are quiescent precursors interposed between myofibers and a sheath of external lamina. Although their activation and recruitment to cycle enable muscle repair and adaptation, the activation signal is not known. Evidence is presented that nitric oxide (NO) mediates satellite cell activation, including morphological hypertrophy and decreased adhesion in the fiber-lamina complex. Activation in vivo occurred within 1 min after injury. Cell isolation and histology showed that pharmacological inhibition of nitric oxide synthase (NOS) activity prevented the immediate injury-induced myogenic cell release and delayed the hypertrophy of satellite cells in that muscle. Transient activation of satellite cells in contralateral muscles 10 min later suggested that a circulating factor may interact with NO-mediated signaling. Interestingly, satellite cell activation in muscles of mdx dystrophic mice and NOS-I knockout mice quantitatively resembled NOS-inhibited release of normal cells, in agreement with reports of displaced and reduced NOS expression in dystrophin-deficient mdx muscle and the complete loss of NOS-I expression in knockout mice. Brief NOS inhibition in normal and mdx mice during injury produced subtle alterations in subsequent repair, including apoptosis in myotube nuclei and myotube formation inside laminar sheaths. Longer NOS inhibition delayed and restricted the extent of repair and resulted in fiber branching. A model proposes the hypothesis that NO release mediates satellite cell activation, possibly via shear-induced rapid increases in NOS activity that produce “NO transients.”

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

Cellular and Molecular Regulation of Muscle Regeneration

2004 ◽  
Vol 84 (1) ◽  
pp. 209-238 ◽  
Author(s):  
SOPHIE B. P. CHARGÉ ◽  
MICHAEL A. RUDNICKI
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Adult Stem Cells ◽  
Cell Activation ◽  
De Novo ◽  
Molecular Regulation ◽  
Muscle Repair ◽  
Adult Skeletal Muscle

Chargé, Sophie B. P., and Michael A. Rudnicki. Cellular and Molecular Regulation of Muscle Regeneration. Physiol Rev 84: 209–238, 2004; 10.1152/physrev.00019.2003.—Under normal circumstances, mammalian adult skeletal muscle is a stable tissue with very little turnover of nuclei. However, upon injury, skeletal muscle has the remarkable ability to initiate a rapid and extensive repair process preventing the loss of muscle mass. Skeletal muscle repair is a highly synchronized process involving the activation of various cellular responses. The initial phase of muscle repair is characterized by necrosis of the damaged tissue and activation of an inflammatory response. This phase is rapidly followed by activation of myogenic cells to proliferate, differentiate, and fuse leading to new myofiber formation and reconstitution of a functional contractile apparatus. Activation of adult muscle satellite cells is a key element in this process. Muscle satellite cell activation resembles embryonic myogenesis in several ways including the de novo induction of the myogenic regulatory factors. Signaling factors released during the regenerating process have been identified, but their functions remain to be fully defined. In addition, recent evidence supports the possible contribution of adult stem cells in the muscle regeneration process. In particular, bone marrow-derived and muscle-derived stem cells contribute to new myofiber formation and to the satellite cell pool after injury.

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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