scholarly journals APitx2-MicroRNA Pathway Modulates Cell Proliferation in Myoblasts and Skeletal-Muscle Satellite Cells and Promotes Their Commitment to a Myogenic Cell Fate

2015 ◽  
Vol 35 (17) ◽  
pp. 2892-2909 ◽  
Author(s):  
Estefanía Lozano-Velasco ◽  
Daniel Vallejo ◽  
Francisco J. Esteban ◽  
Chris Doherty ◽  
Francisco Hernández-Torres ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Cell Fate ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Myogenic Cell ◽  
Quiescent State ◽  
Mirna Pathway ◽  
Microrna Pathway ◽  
Skeletal Muscle Stem Cells

The acquisition of a proliferating-cell status from a quiescent state as well as the shift between proliferation and differentiation are key developmental steps in skeletal-muscle stem cells (satellite cells) to provide proper muscle regeneration. However, how satellite cell proliferation is regulated is not fully understood. Here, we report that the c-isoform of the transcription factor Pitx2 increases cell proliferation in myoblasts by downregulating microRNA 15b (miR-15b), miR-23b, miR-106b, and miR-503. ThisPitx2c-microRNA (miRNA) pathway also regulates cell proliferation in early-activated satellite cells, enhancing Myf5+satellite cells and thereby promoting their commitment to a myogenic cell fate. This study reveals unknown functions of several miRNAs in myoblast and satellite cell behavior and thus may have future applications in regenerative medicine.

scholarly journals Akt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Protein Synthesis ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Proliferation

Skeletal muscle mass is determined by the net dynamic balance between protein synthesis and degradation. Although the Akt/mechanistic target of rapamycin (mTOR)-dependent pathway plays an important role in promoting protein synthesis and subsequent skeletal muscle hypertrophy, the precise molecular regulation of mTOR activity by the upstream protein kinase Akt is largely unknown. In addition, the activation of satellite cells has been indicated as a key regulator of muscle mass. However, the requirement of satellite cells for load-induced skeletal muscle hypertrophy is still under intense debate. In this study, female germline Akt1 knockout (KO) mice were used to examine whether Akt1 deficiency attenuates load-induced skeletal muscle hypertrophy through suppressing mTOR-dependent signaling and satellite cell proliferation. Akt1 KO mice showed a blunted hypertrophic response of skeletal muscle, with a diminished rate of satellite cell proliferation following mechanical overload. In contrast, Akt1 deficiency did not affect the load-induced activation of mTOR signaling and the subsequent enhanced rate of protein synthesis in skeletal muscle. These observations suggest that the load-induced activation of mTOR signaling occurs independently of Akt1 regulation and that Akt1 plays a critical role in regulating satellite cell proliferation during load-induced muscle hypertrophy.

scholarly journals Sox15 Is Required for Skeletal Muscle Regeneration

2004 ◽  
Vol 24 (19) ◽  
pp. 8428-8436 ◽  
Author(s):  
Heon-Jin Lee ◽  
Wolfgang Göring ◽  
Matthias Ochs ◽  
Christian Mühlfeld ◽  
Gerd Steding ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Fate ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Myogenic Cell ◽  
Skeletal Muscle Regeneration ◽  
Term Survival ◽  
Differentiation Potential ◽  
Cell Lineages

ABSTRACT The Sox genes define a family of transcription factors that play a key role in the determination of cell fate during development. The preferential expression of the Sox15 in the myogenic precursor cells led us to suggest that the Sox15 is involved in the specification of myogenic cell lineages or in the regulation of the fusion of myoblasts to form myotubes during the development and regeneration of skeletal muscle. To identify the physiological function of Sox15 in mice, we disrupted the Sox15 by homologous recombination in mice. Sox15-deficient mice were born at expected ratios, were healthy and fertile, and displayed normal long-term survival rates. Histological analysis revealed the normal ultrastructure of myofibers and the presence of comparable amounts of satellite cells in the skeletal muscles of Sox15−/− animals compared to wild-type animals. These results exclude the role of Sox15 in the development of satellite cells. However, cultured Sox15−/− myoblasts displayed a marked delay in differentiation potential in vitro. Moreover, skeletal muscle regeneration in Sox15−/− mice was attenuated after application of a crush injury. These results suggest a requirement for Sox15 in the myogenic program. Expression analyses of the early myogenic regulated factors MyoD and Myf5 showed the downregulation of the MyoD and upregulation of the Myf5 in Sox15−/− myoblasts. These results show an increased proportion of the Myf5-positive cells and suggest a role for Sox15 in determining the early myogenic cell lineages during skeletal muscle development.

Satellite cell proliferation and differentiation during postnatal growth of porcine skeletal muscle

2002 ◽  
Vol 282 (4) ◽  
pp. C899-C906 ◽  
Author(s):  
N. T Mesires ◽  
M. E. Doumit
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Nuclear Antigen ◽  
Positive Staining ◽  
Age Related ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Satellite Cell Proliferation

Age-related changes in satellite cell proliferation and differentiation during rapid growth of porcine skeletal muscle were examined. Satellite cells were isolated from hindlimb muscles of pigs at 1, 7, 14, and 21 wk of age (4 animals/age group). Satellite cells were separated from cellular debris by using Percoll gradient centrifugation and were adsorbed to glass coverslips for fluorescent immunostaining. Positive staining for neural cell adhesion molecule (NCAM) distinguished satellite cells from nonmyogenic cells. The proportion of NCAM-positive cells (satellite cells) in isolates decreased from 1 to 7 wk of age. Greater than 77% of NCAM-positive cells were proliferating cell nuclear antigen positive at all ages studied. Myogenin-positive satellite cells decreased from 30% at 1 wk to 14% at 7 wk of age and remained at constant levels thereafter. These data indicate that a high percentage of satellite cells remain proliferative during rapid postnatal muscle growth. The reduced proportion of myogenin-positive cells during growth may reflect a decrease in the proportion of differentiating satellite cells or accelerated incorporation of myogenin-positive cells into myofibers.

scholarly journals An Overview About the Biology of Skeletal Muscle Satellite Cells

2019 ◽  
Vol 20 (1) ◽  
pp. 24-37 ◽  
Author(s):  
Laura Forcina ◽  
Carmen Miano ◽  
Laura Pelosi ◽  
Antonio Musarò
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Satellite Cell ◽  
Muscle Tissue ◽  
Satellite Cells ◽  
Cell Biology ◽  
Regulatory Networks ◽  
Myogenic Differentiation ◽  
Cell Activity ◽  
Quiescent State

The peculiar ability of skeletal muscle tissue to operate adaptive changes during post-natal development and adulthood has been associated with the existence of adult somatic stem cells. Satellite cells, occupying an exclusive niche within the adult muscle tissue, are considered bona fide stem cells with both stem-like properties and myogenic activities. Indeed, satellite cells retain the capability to both maintain the quiescence in uninjured muscles and to be promptly activated in response to growth or regenerative signals, re-engaging the cell cycle. Activated cells can undergo myogenic differentiation or self-renewal moving back to the quiescent state. Satellite cells behavior and their fate decision are finely controlled by mechanisms involving both cell-autonomous and external stimuli. Alterations in these regulatory networks profoundly affect muscle homeostasis and the dynamic response to tissue damage, contributing to the decline of skeletal muscle that occurs under physio-pathologic conditions. Although the clear myogenic activity of satellite cells has been described and their pivotal role in muscle growth and regeneration has been reported, a comprehensive picture of inter-related mechanisms guiding muscle stem cell activity has still to be defined. Here, we reviewed the main regulatory networks determining satellite cell behavior. In particular, we focused on genetic and epigenetic mechanisms underlining satellite cell maintenance and commitment. Besides intrinsic regulations, we reported current evidences about the influence of environmental stimuli, derived from other cell populations within muscle tissue, on satellite cell biology.

scholarly journals EXERCISE EFFECTS ON MUSCLE STEM CELLS

2018 ◽  
Vol 8 (2) ◽  
pp. 125-135
Author(s):  
Mihaela Jurdana
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Skeletal Muscle Mass ◽  
Exercise Intervention ◽  
Quiescent State ◽  
Muscle Stem Cells ◽  
And Function ◽  
Skeletal Muscle Stem Cells

Satellite cells are skeletal muscle stem cells that facilitate muscle repair and regeneration after “damage” which occurs after physiological stimuli: exercise, post-training micro-injuries and electrical stimulation. Exercise stimuli lead to activation and proliferation of these cells from their quiescent state, therefore, increasing cell numbers having the potential to provide additional myonuclei to their parent muscle fibre or return to a quiescent state. Different exercise modalities are the focus of numerous studies on satellite cells activation. An increase in muscle activity augments satellite cells proliferation as well as skeletal muscle mass and function, both in young and elderly.  This review provides an updated view of the contribution of skeletal muscle satellite cells in regulating skeletal muscle mass and the efficiency of the exercise intervention to attenuate the decline in muscle mass.

The Molecular Responses of Skeletal Muscle Satellite Cells to Continuous Expression of IGF-1: Implications for the Rescue of Induced Muscular Atrophy in Aged Rats

2001 ◽  
Vol 11 (s1) ◽  
pp. S44-S48 ◽  
Author(s):  
Manu V. Chakravarthy ◽  
Frank W. Booth ◽  
Espen E. Spangenburg
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Molecular Mechanisms ◽  
Muscular Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Molecular Evidence ◽  
Igf I ◽  
Satellite Cell Proliferation

Approximately 50% of humans older than 85 years have physical frailty due to weak skeletal muscles. This indicates a need for determining mechanisms to combat this problem. A critical cellular factor for postnatal muscle growth is a population of myogenic precursor cells called satellite cells. Given the complex process of sarcopenia, it has been postulated that, at some point in this process, a limited satellite cell proliferation potential could become rate-limiting to the regrowth of old muscles. It is conceivable that if satellite cell proliferative capacity can be maintained or enhanced with advanced age, sarcopenia could potentially be delayed or prevented. Therefore, the purposes of this paper are to describe whether IGF-I can prevent muscular atrophy induced by repeated cycles of hindlimb immobilization, increase the in vitro proliferation in satellite cells from these muscles and, if so, the molecular mechanisms by which IGF-1 mediates this increased proliferation. Our results provide evidence that IGFI can enhance aged muscle regrowth possibly through increased satellite cell proliferation. The results also suggest that IGF-I enhances satellite cell proliferation by decreasing the cell cycle inhibitor, p27Kip1, through the PI3’-K/Akt pathway. These data provide molecular evidence for IGF-I’s rescue effect upon aging-associated skeletal muscle atrophy.

scholarly journals Reduced Notch signalling leads to postnatal skeletal muscle hypertrophy in Pofut1 cax/cax mice

Open Biology ◽  
2016 ◽  
Vol 6 (9) ◽  
pp. 160211 ◽  
Author(s):  
Bilal Al Jaam ◽  
Katy Heu ◽  
Florian Pennarubia ◽  
Alexandre Segelle ◽  
Laetitia Magnol ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Target Genes ◽  
Muscle Growth ◽  
Notch Signalling ◽  
Quiescent State ◽  
Notch Receptors

Postnatal skeletal muscle growth results from the activation of satellite cells and/or an increase in protein synthesis. The Notch signalling pathway maintains satellite cells in a quiescent state, and once activated, sustains their proliferation and commitment towards differentiation. In mammals, POFUT1-mediated O -fucosylation regulates the interactions between NOTCH receptors and ligands of the DELTA/JAGGED family, thus initiating the activation of canonical Notch signalling. Here, we analysed the consequences of downregulated expression of the Pofut1 gene on postnatal muscle growth in mutant Pofut1 cax/cax (cax, compact axial skeleton) mice and differentiation of their satellite cell-derived myoblasts (SCDMs). Pofut1 cax/cax mice exhibited muscle hypertrophy, no hyperplasia and a decrease in satellite cell numbers compared with wild-type C3H mice. In agreement with these observations, Pofut1 cax/cax SCDMs differentiated earlier concomitant with reduced Pax7 expression and decrease in PAX7 + /MYOD − progenitor cells. In vitro binding assays showed a reduced interaction of DELTA-LIKE 1 ligand (DLL1) with NOTCH receptors expressed at the cell surface of SCDMs, leading to a decreased Notch signalling as seen by the quantification of cleaved NICD and Notch target genes. These results demonstrated that POFUT1-mediated O- fucosylation of NOTCH receptors regulates myogenic cell differentiation and affects postnatal muscle growth in mice.

scholarly journals microRNA-1 and microRNA-206 regulate skeletal muscle satellite cell proliferation and differentiation by repressing Pax7

2010 ◽  
Vol 190 (5) ◽  
pp. 867-879 ◽  
Author(s):  
Jian-Fu Chen ◽  
Yazhong Tao ◽  
Juan Li ◽  
Zhongliang Deng ◽  
Zhen Yan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Cell Differentiation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Adult Stem Cells ◽  
Myoblast Differentiation ◽  
Proliferative Potential ◽  
Satellite Cell Proliferation

Skeletal muscle satellite cells are adult stem cells responsible for postnatal skeletal muscle growth and regeneration. Paired-box transcription factor Pax7 plays a central role in satellite cell survival, self-renewal, and proliferation. However, how Pax7 is regulated during the transition from proliferating satellite cells to differentiating myogenic progenitor cells is largely unknown. In this study, we find that miR-1 and miR-206 are sharply up-regulated during satellite cell differentiation and down-regulated after muscle injury. We show that miR-1 and miR-206 facilitate satellite cell differentiation by restricting their proliferative potential. We identify Pax7 as one of the direct regulatory targets of miR-1 and miR-206. Inhibition of miR-1 and miR-206 substantially enhances satellite cell proliferation and increases Pax7 protein level in vivo. Conversely, sustained Pax7 expression as a result of the loss of miR-1 and miR-206 repression elements at its 3′ untranslated region significantly inhibits myoblast differentiation. Therefore, our experiments suggest that microRNAs participate in a regulatory circuit that allows rapid gene program transitions from proliferation to differentiation.

scholarly journals Functional Overload Enhances Satellite Cell Properties in Skeletal Muscle

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Shin Fujimaki ◽  
Masanao Machida ◽  
Tamami Wakabayashi ◽  
Makoto Asashima ◽  
Tohru Takemasa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Physical Exercise ◽  
Resistance Exercise ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Quiescent State ◽  
Proliferative Capacity ◽  
Differentiation Potential ◽  
Activated State

Skeletal muscle represents a plentiful and accessible source of adult stem cells. Skeletal-muscle-derived stem cells, termed satellite cells, play essential roles in postnatal growth, maintenance, repair, and regeneration of skeletal muscle. Although it is well known that the number of satellite cells increases following physical exercise, functional alterations in satellite cells such as proliferative capacity and differentiation efficiency following exercise and their molecular mechanisms remain unclear. Here, we found that functional overload, which is widely used to model resistance exercise, causes skeletal muscle hypertrophy and converts satellite cells from quiescent state to activated state. Our analysis showed that functional overload induces the expression of MyoD in satellite cells and enhances the proliferative capacity and differentiation potential of these cells. The changes in satellite cell properties coincided with the inactivation of Notch signaling and the activation of Wnt signaling and likely involve modulation by transcription factors of the Sox family. These results indicate the effects of resistance exercise on the regulation of satellite cells and provide insight into the molecular mechanism of satellite cell activation following physical exercise.

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