Caspase 3 cleavage of Pax7 inhibits self-renewal of satellite cells

Dick, Sarah A.; Chang, Natasha C.; Dumont, Nicolas A.; Bell, Robert; Putinski, Charis; Kawabe, Yoichi; Litchfield, David W.; Rudnicki, Michael A.; Megeney, Lynn A.

doi:10.1073/pnas.1512869112

Cited by 72 publications

(71 citation statements)

References 32 publications

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“…9 J ) post‐PEMF exposure. Caspases‐3 and ‐9 and Bcl‐xL have been shown to synergize to promote myogenesis (44, 45), whereby Caspase‐3 stops the expansion of satellite cells (45). Accordingly, cleaved Caspases 3 and 9 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Ambient and supplemental magnetic fields promote myogenesis via a TRPC1‐mitochondrial axis: evidence of a magnetic mitohormetic mechanism

Yap¹,

Tai²,

Fröhlich

et al. 2019

The FASEB Journal

138

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We show that both supplemental and ambient magnetic fields modulate myogenesis. A lone 10 min exposure of myoblasts to 1.5 mT amplitude supplemental pulsed magnetic fields (PEMFs) accentuated in vitro myogenesis by stimulating transient receptor potential (TRP)‐C1‐mediated calcium entry and downstream nuclear factor of activated T cells (NFAT)‐transcriptional and P300/CBP‐associated factor (PCAF)‐epigenetic cascades, whereas depriving myoblasts of ambient magnetic fields slowed myogenesis, reduced TRPC1 expression, and silenced NFAT‐transcriptional and PCAF‐epigenetic cascades. The expression levels of peroxisome proliferatoractivated receptor g coactivator 1α, the master regulator of mitochondriogenesis, was also enhanced by brief PEMF exposure. Accordingly, mitochondriogenesis and respiratory capacity were both enhanced with PEMF exposure, paralleling TRPC1 expression and pharmacological sensitivity. Clustered regularly interspaced short palindromic repeats‐Cas9 knockdown of TRPC1 precluded proliferative and mitochondrial responses to supplemental PEMFs, whereas small interfering RNA gene silencing of TRPM7 did not, coinciding with data that magnetoreception did not coincide with the expression or function of other TRP channels. The aminoglycoside antibiotics antagonized and down‐regulated TRPC1 expression and, when applied concomitantly with PEMF exposure, attenuated PEMF‐stimulated calcium entry, mitochondrial respiration, proliferation, differentiation, and epigenetic directive in myoblasts, elucidating why the developmental potential of magnetic fields may have previously escaped detection. Mitochondrial‐based survival adaptations were also activated upon PEMF stimulation. Magnetism thus deploys an authentic myogenic directive that relies on an interplay between mitochondria and TRPC1 to reach fruition.—Yap, J. L. Y., Tai, Y. K., Fröhlich, J., Fong, C. H. H., Yin, J. N., Foo, Z. L., Ramanan, S., Beyer, C., Toh, S. J., Casarosa, M., Bharathy, N., Kala, M. P., Egli, M., Taneja, R., Lee, C. N., Franco‐Obregón, A. Ambient and supplemental magnetic fields promote myogenesis via a TRPC1‐mitochondrial axis: evidence of a magnetic mitohormetic mechanism. FASEB J. 33, 12853–12872 (2019). http://www.fasebj.org

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Section: Resultsmentioning

confidence: 99%

Ambient and supplemental magnetic fields promote myogenesis via a TRPC1‐mitochondrial axis: evidence of a magnetic mitohormetic mechanism

Yap¹,

Tai²,

Fröhlich

et al. 2019

The FASEB Journal

138

View full text Add to dashboard Cite

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“…Caspase-3 activation has been shown to be involved in impairment of satellite cell renewal and participate in apoptotic events during muscle repair in mitochondrial diseases2627. Moreover, enhanced apoptosis and proteasome activity have been implicated in the pathology of MDC1A1328.…”

Section: Resultsmentioning

confidence: 99%

Bioenergetic Impairment in Congenital Muscular Dystrophy Type 1A and Leigh Syndrome Muscle Cells

Fontes-Oliveira

Steinz

Schneiderat³

et al. 2017

Sci Rep

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Skeletal muscle has high energy requirement and alterations in metabolism are associated with pathological conditions causing muscle wasting and impaired regeneration. Congenital muscular dystrophy type 1A (MDC1A) is a severe muscle disorder caused by mutations in the LAMA2 gene. Leigh syndrome (LS) is a neurometabolic disease caused by mutations in genes related to mitochondrial function. Skeletal muscle is severely affected in both diseases and a common feature is muscle weakness that leads to hypotonia and respiratory problems. Here, we have investigated the bioenergetic profile in myogenic cells from MDC1A and LS patients. We found dysregulated expression of genes related to energy production, apoptosis and proteasome in myoblasts and myotubes. Moreover, impaired mitochondrial function and a compensatory upregulation of glycolysis were observed when monitored in real-time. Also, alterations in cell cycle populations in myoblasts and enhanced caspase-3 activity in myotubes were observed. Thus, we have for the first time demonstrated an impairment of the bioenergetic status in human MDC1A and LS muscle cells, which could contribute to cell cycle disturbance and increased apoptosis. Our findings suggest that skeletal muscle metabolism might be a promising pharmacological target in order to improve muscle function, energy efficiency and tissue maintenance of MDC1A and LS patients.

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“…The total number of cells was significantly decreased in CD82-sh compared to control-sh cultures (t-test p<0.03). Apoptosis assays utilized Annexin V detection (D), since caspase 3 activity can regulate other functions, including self-renewal of satellite cells (Dick et al, 2015). No significant differences in apoptosis were seen between control- and CD82-sh cultures.…”

Section: Figurementioning

confidence: 99%

CD82 Is a Marker for Prospective Isolation of Human Muscle Satellite Cells and Is Linked to Muscular Dystrophies

et al. 2016

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Summary Cell surface markers for prospective isolation of stem cells from human skeletal muscle have been difficult to identify. Such markers would be powerful tools for studying satellite cell function during homeostasis and in pathogenesis of diseases such as muscular dystrophies. In this study, we show that the tetraspanin KAI/CD82 is an excellent marker for prospectively isolating stem cells from human fetal and adult skeletal muscle. Human CD82+ muscle cells robustly engraft into a mouse model of muscular dystrophy. shRNA knockdown of CD82 in myogenic cells reduces myoblast proliferation, suggesting it is functionally involved in muscle homeostasis. CD82 physically interacts with alpha7beta1 integrin (α7β1-ITG) and with α-sarcoglycan, a member of the Dystrophin-Associated Glycoprotein Complex (DAPC), both of which have been linked to muscular dystrophies. Consistently, CD82 expression is decreased in Duchenne muscular dystrophy patients, together suggesting that CD82 function may be important for muscle stem cell function in muscular disorders.

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Caspase 3 cleavage of Pax7 inhibits self-renewal of satellite cells

Cited by 72 publications

References 32 publications

Ambient and supplemental magnetic fields promote myogenesis via a TRPC1‐mitochondrial axis: evidence of a magnetic mitohormetic mechanism

Ambient and supplemental magnetic fields promote myogenesis via a TRPC1‐mitochondrial axis: evidence of a magnetic mitohormetic mechanism

Bioenergetic Impairment in Congenital Muscular Dystrophy Type 1A and Leigh Syndrome Muscle Cells

CD82 Is a Marker for Prospective Isolation of Human Muscle Satellite Cells and Is Linked to Muscular Dystrophies

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