Effect of growth selection of broilers on breast muscle satellite cell function: Response of satellite cells to NOV, COMP, MYBP-C1, and CSRP3

Abstract PAX7 is a paired-homeobox transcription factor that specifies the myogenic identity of muscle stem cells and acts as a nodal factor by stimulating proliferation while inhibiting differentiation. We previously found that PAX7 recruits the H3K4 methyltransferases MLL1/2 to epigenetically activate target genes. Here we report that in the absence of Mll1, myoblasts exhibit reduced H3K4me3 at both Pax7 and Myf5 promoters and reduced Pax7 and Myf5 expression. Mll1-deficient myoblasts fail to proliferate but retain their differentiation potential, while deletion of Mll2 had no discernable effect. Re-expression of PAX7 in committed Mll1 cKO myoblasts restored H3K4me3 enrichment at the Myf5 promoter and Myf5 expression. Deletion of Mll1 in satellite cells reduced satellite cell proliferation and self-renewal, and significantly impaired skeletal muscle regeneration. Pax7 expression was unaffected in quiescent satellite cells but was markedly downregulated following satellite cell activation. Therefore, MLL1 is required for PAX7 expression and satellite cell function in vivo. Furthermore, PAX7, but not MLL1, is required for Myf5 transcriptional activation in committed myoblasts.

Download Full-text

Stem cells for skeletal muscle repair

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2011.0027 ◽

2011 ◽

Vol 366 (1575) ◽

pp. 2297-2306 ◽

Cited By ~ 63

Author(s):

Jennifer L. Shadrach ◽

Amy J. Wagers

Keyword(s):

Skeletal Muscle ◽

Stem Cells ◽

Satellite Cell ◽

Satellite Cells ◽

Cell Function ◽

Therapeutic Potential ◽

Muscle Disease ◽

Muscle Fibres ◽

Muscle Repair ◽

Muscle Satellite Cells

Skeletal muscle is a highly specialized tissue composed of non-dividing, multi-nucleated muscle fibres that contract to generate force in a controlled and directed manner. Skeletal muscle is formed during embryogenesis from a subset of muscle precursor cells, which generate both differentiated muscle fibres and specialized muscle-forming stem cells known as satellite cells. Satellite cells remain associated with muscle fibres after birth and are responsible for muscle growth and repair throughout life. Failure in satellite cell function can lead to delayed, impaired or failed recovery after muscle injury, and such failures become increasingly prominent in cases of progressive muscle disease and in old age. Recent progress in the isolation of muscle satellite cells and elucidation of the cellular and molecular mediators controlling their activity indicate that these cells represent promising therapeutic targets. Such satellite cell-based therapies may involve either direct cell replacement or development of drugs that enhance endogenous muscle repair mechanisms. Here, we discuss recent breakthroughs in understanding both the cell intrinsic and extrinsic regulators that determine the formation and function of muscle satellite cells, as well as promising paths forward to realizing their full therapeutic potential.

Download Full-text

Skeletal muscle satellite cell diversity: Satellite cells form fibers of different types in cell culture

Developmental Biology ◽

10.1016/0012-1606(91)90083-f ◽

1991 ◽

Vol 143 (2) ◽

pp. 320-334 ◽

Cited By ~ 107

Author(s):

Jeffrey L. Feldman ◽

Frank E. Stockdale

Keyword(s):

Skeletal Muscle ◽

Cell Culture ◽

Satellite Cell ◽

Satellite Cells ◽

Muscle Satellite Cell ◽

Different Types ◽

Cell Diversity ◽

Skeletal Muscle Satellite Cell

Download Full-text

Molecular Regulation and Rejuvenation of Muscle Stem (Satellite) Cell Aging

The Indonesian Biomedical Journal ◽

10.18585/inabj.v7i2.73 ◽

2015 ◽

Vol 7 (2) ◽

pp. 73

Author(s):

Anna Meiliana ◽

Nurrani Mustika Dewi ◽

Andi Wijaya

Keyword(s):

Skeletal Muscle ◽

Stem Cells ◽

Stem Cell ◽

Satellite Cell ◽

Muscle Mass ◽

Satellite Cells ◽

Cell Function ◽

Muscle Stem Cell ◽

Muscle Aging ◽

Age Related

BACKGROUND: Age-related muscle loss leads to lack of muscle strength, resulting in reduced posture and mobility and an increased risk of falls, all of which contribute to a decrease in quality of life. Skeletal muscle regeneration is a complex process, which is not yet completely understood.CONTENT: Skeletal muscle undergoes a progressive age-related loss in mass and function. Preservation of muscle mass depends in part on satellite cells, the resident stem cells of skeletal muscle. Reduced satellite cell function may contribute to the age-associated decrease in muscle mass. Recent studies have delineated that the aging process in organ stem cells is largely caused by age-specific changes in the differentiated niches, and that regenerative outcomes often depend on the age of the niche, rather than on stem cell age. It is likely that epigenetic states will be better define such key satellite cell features as prolonged quiescence and lineage fidelity. It is also likely that DNA and histone modifications will underlie many of the changes in aged satellite cells that account for age-related declines in functionality and rejuvenation through exposure to the systemic environment.SUMMARY: Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Decreased muscle stem cell function in aging has long been shown to depend on altered environmental cues, whereas the contribution of intrinsic mechanisms remained less clear. Signals in the aged niche were shown to cause permanent defects in the ability of satellite cells to return to quiescence, ultimately also impairing the maintenance of self-renewing satellite cells. Therefore, only anti-aging strategies taking both factors, the stem cell niche and the stem cells per se, into consideration may ultimately be successful.KEYWORDS: satellite cell, muscle, aging, niche, regenerations

Download Full-text

Delay in post-ovariectomy estrogen replacement negates estrogen-induced augmentation of post-exercise muscle satellite cell proliferation

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2015-0106 ◽

2015 ◽

Vol 93 (11) ◽

pp. 945-951 ◽

Cited By ~ 2

Author(s):

Gary Mangan ◽

Sobia Iqbal ◽

Andrew Hubbard ◽

Victoria Hamilton ◽

Eric Bombardier ◽

...

Keyword(s):

Cell Proliferation ◽

Satellite Cell ◽

Satellite Cells ◽

Estrogen Replacement ◽

Sprague Dawley ◽

Muscle Satellite Cell ◽

Post Exercise ◽

Muscle Satellite Cells ◽

Satellite Cell Proliferation ◽

Exercise Muscle

This study examined the effects of a delay in post-ovariectomy replacement of 17β-estradiol (estrogen) on the post-exercise proliferation of muscle satellite cells. Nine-week-old, ovariectomized, female Sprague–Dawley rats (n = 64) were distributed among 8 groups based on estrogen status (0.25 mg estrogen pellet or sham), exercise status (90 min run at 17 m·min–1 and a grade of –13.5° or unexercised), and estrogen replacement (“proximal”, estrogen replacement within 2 weeks; or “delayed”, estrogen replacement at 11 weeks following ovariectomy). Significant increases in satellite cells were found in the soleus and white gastrocnemius muscle (immunofluorescent colocalization of nuclei with Pax7) 72 h following eccentric exercise (p < 0.05) in all exercised groups. Proximal E2 replacement resulted in a further augmentation of muscle satellite cells in exercised rats (p < 0.05) relative to the delayed estrogen replacement group. Expression of PI3K was unaltered and phosphorylation of Akt relative to total Akt increased following estrogen supplementation and exercise. Exercise alone did not alter the expression levels of Akt. An 11 week delay in post-ovariectomy estrogen replacement negated the augmenting influence seen with proximal (2 week delay) post-ovariectomy estrogen replacement on post-exercise muscle satellite cell proliferation. This effect appears to be independent of the PI3K–Akt signaling pathway.

Download Full-text

Brain-derived Neurotrophic Factor Regulates Satellite Cell Differentiation and Skeltal Muscle Regeneration

Molecular Biology of the Cell ◽

10.1091/mbc.e10-02-0154 ◽

2010 ◽

Vol 21 (13) ◽

pp. 2182-2190 ◽

Cited By ~ 73

Author(s):

Charlene Clow ◽

Bernard J. Jasmin

Keyword(s):

Skeletal Muscle ◽

Satellite Cell ◽

Satellite Cells ◽

Neurotrophic Factor ◽

Cell Function ◽

Brain Derived Neurotrophic Factor ◽

Postnatal Growth ◽

Adult Skeletal Muscle

In adult skeletal muscle, brain-derived neurotrophic factor (BDNF) is expressed in myogenic progenitors known as satellite cells. To functionally address the role of BDNF in muscle satellite cells and regeneration in vivo, we generated a mouse in which BDNF is specifically depleted from skeletal muscle cells. For comparative purposes, and to determine the specific role of muscle-derived BDNF, we also examined muscles of the complete BDNF−/− mouse. In both models, expression of the satellite cell marker Pax7 was significantly decreased. Furthermore, proliferation and differentiation of primary myoblasts was abnormal, exhibiting delayed induction of several markers of differentiation as well as decreased myotube size. Treatment with exogenous BDNF protein was sufficient to rescue normal gene expression and myotube size. Because satellite cells are responsible for postnatal growth and repair of skeletal muscle, we next examined whether regenerative capacity was compromised. After injury, BDNF-depleted muscle showed delayed expression of several molecular markers of regeneration, as well as delayed appearance of newly regenerated fibers. Recovery of wild-type BDNF levels was sufficient to restore normal regeneration. Together, these findings suggest that BDNF plays an important role in regulating satellite cell function and regeneration in vivo, particularly during early stages.

Download Full-text

Canonical NF-κB signaling regulates satellite stem cell homeostasis and function during regenerative myogenesis

Journal of Molecular Cell Biology ◽

10.1093/jmcb/mjy053 ◽

2018 ◽

Vol 11 (1) ◽

pp. 53-66 ◽

Cited By ~ 3

Author(s):

Alex R Straughn ◽

Sajedah M Hindi ◽

Guangyan Xiong ◽

Ashok Kumar

Keyword(s):

Skeletal Muscle ◽

Satellite Cell ◽

Satellite Cells ◽

Muscle Regeneration ◽

Cell Function ◽

Skeletal Muscle Regeneration ◽

Cell Homeostasis ◽

Adult Skeletal Muscle ◽

Adult Mice ◽

And Function

Abstract Skeletal muscle regeneration in adults is attributed to the presence of satellite stem cells that proliferate, differentiate, and eventually fuse with injured myofibers. However, the signaling mechanisms that regulate satellite cell homeostasis and function remain less understood. While IKKβ-mediated canonical NF-κB signaling has been implicated in the regulation of myogenesis and skeletal muscle mass, its role in the regulation of satellite cell function during muscle regeneration has not been fully elucidated. Here, we report that canonical NF-κB signaling is induced in skeletal muscle upon injury. Satellite cell-specific inducible ablation of IKKβ attenuates skeletal muscle regeneration in adult mice. Targeted ablation of IKKβ also reduces the number of satellite cells in injured skeletal muscle of adult mice, potentially through inhibiting their proliferation and survival. We also demonstrate that the inhibition of specific components of the canonical NF-κB pathway causes precocious differentiation of cultured satellite cells both ex vivo and in vitro. Finally, our results highlight that the constitutive activation of canonical NF-κB signaling in satellite cells also attenuates skeletal muscle regeneration following injury in adult mice. Collectively, our study demonstrates that the proper regulation of canonical NF-κB signaling is important for the regeneration of adult skeletal muscle.

Download Full-text

Recent Developments in Breast Muscle Myopathies Associated with Growth in Poultry

Annual Review of Animal Biosciences ◽

10.1146/annurev-animal-020518-115311 ◽

2019 ◽

Vol 7 (1) ◽

pp. 289-308 ◽

Cited By ~ 10

Author(s):

Sandra G. Velleman

Keyword(s):

Skeletal Muscle ◽

Stem Cell ◽

Satellite Cell ◽

Meat Quality ◽

Satellite Cells ◽

Muscle Development ◽

Growth Function ◽

Repair Process ◽

Breast Muscle ◽

Cellular Mechanisms

The functional unit in skeletal muscle is the multinucleated myofiber, which is composed of parallel arrays of microfibrils. The myofiber and sarco-mere structure of skeletal muscle are established during embryogenesis, when mononuclear myoblast cells fuse to form multinucleated myotubes and develop into muscle fibers. With the myoblasts permanently unable to enter a proliferative state again after they fuse to form the multinucleated myotube, postnatal myofiber growth, muscle homeostasis, and myofiber regeneration are dependent on a myogenic stem cell, the satellite cell. Because the satellite cell is a partially differentiated stem cell controlling the state of skeletal muscle structure throughout the life of the bird, it can impact muscle development and structure, growth, and regeneration and, subsequently, meat quality. When myofibers are damaged, muscle repair is dependent on the satellite cells. Regenerated myofibers after the repair process should be similar to the original muscle fiber. Despite significant improvements in meat-type birds, degenerative myopathies have arisen. In many of these degenerative breast muscle myopathies, like Wooden Breast, satellite cell–mediated regeneration of muscle is suppressed. Thus, the biological function of avian myogenic satellite cells and their influence on cellular mechanisms affecting breast muscle development and growth, function during degenerative myopathies, and meat quality are discussed.

Download Full-text