scholarly journals Loss of Ptpn11 (Shp2) drives satellite cells into quiescence

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Joscha Griger ◽  
Robin Schneider ◽  
Ines Lahmann ◽  
Verena Schöwel ◽  
Charles Keller ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tyrosine Phosphatase ◽  
Muscle Growth ◽  
Cell Activity ◽  
Muscle Stem Cells ◽  
Myogenic Stem Cells ◽  
Postnatal Myogenesis ◽  
Receptor Tyrosine Phosphatase ◽  
Satellite Cell Activity

The equilibrium between proliferation and quiescence of myogenic progenitor and stem cells is tightly regulated to ensure appropriate skeletal muscle growth and repair. The non-receptor tyrosine phosphatase Ptpn11 (Shp2) is an important transducer of growth factor and cytokine signals. Here we combined complex genetic analyses, biochemical studies and pharmacological interference to demonstrate a central role of Ptpn11 in postnatal myogenesis of mice. Loss of Ptpn11 drove muscle stem cells out of the proliferative and into a resting state during muscle growth. This Ptpn11 function was observed in postnatal but not fetal myogenic stem cells. Furthermore, muscle repair was severely perturbed when Ptpn11 was ablated in stem cells due to a deficit in stem cell proliferation and survival. Our data demonstrate a molecular difference in the control of cell cycle withdrawal in fetal and postnatal myogenic stem cells, and assign to Ptpn11 signaling a key function in satellite cell activity.

The COX-2 pathway regulates growth of atrophied muscle via multiple mechanisms

2006 ◽  
Vol 290 (6) ◽  
pp. C1651-C1659 ◽  
Author(s):  
Brenda A. Bondesen ◽  
Stephen T. Mills ◽  
Grace K. Pavlath
Keyword(s):  
Muscle Mass ◽  
Muscle Regeneration ◽  
Muscle Growth ◽  
Cell Activity ◽  
Hindlimb Suspension ◽  
Normal Muscle ◽  
Cox 2 ◽  
Proliferation In Vitro

Loss of muscle mass occurs with disease, injury, aging, and inactivity. Restoration of normal muscle mass depends on myofiber growth, the regulation of which is incompletely understood. Cyclooxygenase (COX)-2 is one of two isoforms of COX that catalyzes the synthesis of prostaglandins, paracrine hormones that regulate diverse physiological and pathophysiological processes. Previously, we demonstrated that the COX-2 pathway regulates early stages of myofiber growth during muscle regeneration. However, whether the COX-2 pathway plays a common role in adult myofiber growth or functions specifically during muscle regeneration is unknown. Therefore, we examined the role of COX-2 during myofiber growth following atrophy in mice. Muscle atrophy was induced by hindlimb suspension (HS) for 2 wk, followed by a reloading period, during which mice were treated with either the COX-2-selective inhibitor SC-236 (6 mg·kg−1·day−1) or vehicle. COX-2 protein was expressed and SC-236 attenuated myofiber growth during reloading in both soleus and plantaris muscles. Attenuated myofiber growth in the soleus was associated with both decreased myonuclear addition and decreased inflammation, whereas neither of these processes mediated the effects of SC-236 on plantaris growth. In addition, COX-2−/− satellite cells exhibited impaired activation/proliferation in vitro, suggesting direct regulation of muscle cell activity by COX-2. Together, these data suggest that the COX-2 pathway plays a common regulatory role during various types of muscle growth via multiple mechanisms.

The role of receptor protein tyrosine phosphatase α in neuronal differentiation of embryonic stem cells

1996 ◽  
Vol 91 (2) ◽  
pp. 304-307 ◽  
Author(s):  
Wouter G. van Inzen ◽  
Maikel P. Peppelenbosch ◽  
Maria W.M. van den Brand ◽  
Leon G.J. Tertoolen ◽  
Siegfried de Laat
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Neuronal Differentiation ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Embryonic Stem ◽  
Receptor Protein ◽  
Protein Tyrosine ◽  
Receptor Protein Tyrosine Phosphatase

Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans

2007 ◽  
Vol 102 (6) ◽  
pp. 2232-2239 ◽  
Author(s):  
Marcas M. Bamman ◽  
John K. Petrella ◽  
Jeong-su Kim ◽  
David L. Mayhew ◽  
James M. Cross
Keyword(s):  
Cluster Analysis ◽  
Human Subjects ◽  
Cell Activity ◽  
Differentially Expressed ◽  
Entire Cohort ◽  
Specific Factors ◽  
First Time ◽  
Muscle Biopsies ◽  
Satellite Cell Activity

We applied K-means cluster analysis to test the hypothesis that muscle-specific factors known to modulate protein synthesis and satellite cell activity would be differentially expressed during progressive resistance training (PRT, 16 wk) in 66 human subjects experiencing extreme, modest, and failed myofiber hypertrophy. Muscle mRNA expression of IGF-I isoform Ea (IGF-IEa), mechanogrowth factor (MGF, IGF-IEc), myogenin, and MyoD were assessed in muscle biopsies collected at baseline (T1) and 24 h after the first (T2) and last (T3) loading bouts from previously untrained subjects clustered as extreme responders (Xtr, n = 17), modest responders (Mod, n = 32), and nonresponders (Non, n = 17) based on mean myofiber hypertrophy. Myofiber growth averaged 2,475 μm2 in Xtr, 1,111 μm2 in Mod, and −16 μm2 in Non. Main training effects revealed increases in all transcripts (46–83%, P < 0.005). For the entire cohort, IGF-IEa, MGF, and myogenin mRNAs were upregulated by T2 ( P < 0.05), while MyoD did not increase significantly until T3 ( P < 0.001). Within clusters, MGF and myogenin upregulation was robust in Xtr (126% and 65%) and Mod (73% and 41%) vs. no changes in Non. While significant in all clusters by T3, IGF-IEa increased most in Xtr (105%) and least in Non (44%). Although MyoD expression increased overall, no changes within clusters were detected. We reveal for the first time that MGF and myogenin transcripts are differentially expressed in subjects experiencing varying degrees of PRT-mediated myofiber hypertrophy. The data strongly suggest the load-mediated induction of these genes may initiate important actions necessary to promote myofiber growth during PRT, while the role of MyoD is less clear.

scholarly journals Gene Expression Profiling of Muscle Stem Cells Identifies Novel Regulators of Postnatal Myogenesis

2016 ◽  
Vol 4 ◽  
Author(s):  
Sonia Alonso-Martin ◽  
Anne Rochat ◽  
Despoina Mademtzoglou ◽  
Jessica Morais ◽  
Aurélien de Reyniès ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Muscle Stem Cells ◽  
Postnatal Myogenesis
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