Muscle PGC-1α modulates satellite cell number and proliferation by remodeling the stem cell niche

Dinulovic, Ivana; Furrer, Regula; Beer, Markus; Ferry, Arnaud; Cardel, Bettina; Handschin, Christoph

doi:10.1186/s13395-016-0111-9

Cited by 32 publications

(39 citation statements)

References 29 publications

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“…Importantly, even though a strong anti-inflammatory pattern of cytokine expression representing an M2-type polarization is observed, the less robust increase in M1, pro-inflammatory cytokine suggests that muscle PGC-1α could generally prime macrophages for rapid action, in which an M1 to M2 transition has to be tightly orchestrated to ensure proper repair and regeneration. An increased regenerative capacity in muscles overexpressing PGC-1α has recently been postulated15. We have shown that in addition to the increase of PGC-1α expression immediately and 4 h post-exercise, the expression of several chemokines and cytokines was also elevated 0 h and 4 h after exercise.…”

Section: Discussionmentioning

confidence: 55%

“…Muscle PGC-1α could thereby be indicative of the higher resistance of trained muscle fibers against damage and the more efficient repair and regeneration process1819 in a physiological context with consistently elevated PGC-1α gene expression. Indeed, the higher proliferative rate of satellite cells in MCKα mice further supports this hypothesis15. However, the exact chain of events will have to be elucidated in a temporal analysis in animal models in vivo after acute exercise and chronic training that both reflect the pulsatile induction of PGC-1α after each exercise bout and the persistent increase in basal PGC-1α expression linked to the fiber-type switch after prolonged endurance training20.…”

Section: Discussionmentioning

confidence: 90%

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Paracrine cross-talk between skeletal muscle and macrophages in exercise by PGC-1α-controlled BNP

Furrer

Eisele

Schmidt

et al. 2017

Sci Rep

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Activation of resident and infiltrating immune cells is a central event in training adaptation and other contexts of skeletal muscle repair and regeneration. A precise orchestration of inflammatory events in muscle fibers and immune cells is required after recurrent contraction-relaxation cycles. However, the mechanistic aspects of this important regulation remain largely unknown. We now demonstrate that besides a dominant role in controlling cellular metabolism, the peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) also has a profound effect on cytokine expression in muscle tissue. Muscle PGC-1α expression results in activation of tissue-resident macrophages, at least in part mediated by PGC-1α-dependent B-type natriuretic peptide (BNP) production and secretion. Positive effects of exercise in metabolic diseases and other pathologies associated with chronic inflammation could accordingly involve the PGC-1α-BNP axis and thereby provide novel targets for therapeutic approaches.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 90%

Paracrine cross-talk between skeletal muscle and macrophages in exercise by PGC-1α-controlled BNP

Furrer

Eisele

Schmidt

et al. 2017

Sci Rep

Self Cite

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“…Considering the selective attenuation of extrasynaptic utrophin in the Sol muscles of MKO animals and the significant mitochondrial defects in MKO mice (38), it is likely that this translocation of PGC‐1α to the membrane represents a cellular adjustment to maintain sarcolemmal utrophin levels and subsarcolemmal mitochondrial gene expression in EDL muscles specifically. Additionally, PGC‐1α modulates other aspects of the sarcolemmal environment, including inducing critical components of the satellite cell niche fibronectin and tenascin C (73). Thus, enhanced local PGC‐1α activity may compensate for the lack of AMPK in administering the sarcolemmal compartment.…”

Section: Discussionmentioning

confidence: 99%

The role of AMP‐activated protein kinase in the expression of the dystrophin‐associated protein complex in skeletal muscle

et al. 2018

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Stimulation of AMPK induces the expression of dystrophin-associated protein complex (DAPC) components in skeletal muscle, whereas reductions in AMPK are associated with DAPC dysfunction. We sought to determine whether AMPK was necessary for the maintenance of DAPC expression in skeletal muscle. Fast, glycolytic extensor digitorum longus (EDL) and slow, oxidative soleus (Sol) muscles from wild-type mice and from littermates with skeletal muscle-specific knockout of the AMPK β1 and β2 subunits (AMPK β1 β2M-KO; MKO) were analyzed. DAPC mRNA and protein expression were similar between genotypes, with the exception of elevated neuronal nitric oxide synthase expression at the sarcolemma in MKO muscles. The content of transcriptional and post-transcriptional regulators of the DAPC was also not affected by the loss of AMPK. However, MyoD and myogenin expression was diminished in MKO muscles, consistent with previous reports of myopathy in these animals. Furthermore, we observed decrements in extrasynaptic utrophin expression selectively in MKO Sol muscles, likely due to the adaptive accumulation of peroxisome proliferator-activated receptor γ coactivator-1α at the sarcolemma of MKO EDL muscles. Collectively, the evidence indicates that AMPK is sufficient but not essential for the maintenance of DAPC expression in skeletal muscle, yet it is required for preserving extrasynaptic utrophin levels in slow oxidative muscles.-Dial, A. G., Rooprai, P., Lally, J. S., Bujak, A. L., Steinberg, G. R., Ljubicic, V. The role of AMP-activated protein kinase in the expression of the dystrophin-associated protein complex in skeletal muscle.

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“…In particular, PGC-1 null satellite cells have a higher propensity for activation and proliferation [45]. …”

Section: Satellite Cellsmentioning

confidence: 99%

Muscle stem cell and physical activity: what point is the debate at?

et al. 2017

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AbstractIn the last 15 years, it emerged that the practice of regular physical activity reduces the risks of many diseases (cardiovascular diseases, diabetes, etc.) and it is fundamental in weight control and energy consuming to contrast obesity. Different groups proposed many molecular mechanisms as responsible for the positive effects of physical activity in healthy life. However, many points remain to be clarified. In this mini-review we reported the latest observations on the effects of physical exercise on healthy skeletal and cardiac muscle focusing on muscle stem cells. The last ones represent the fundamental elements for muscle regeneration post injury, but also for healthy muscle homeostasis.Interestingly, in both muscle tissues the morphological consequence of physical activity is a physiological hypertrophy that depends on different phenomena both in differentiated cells and stem cells. The signaling pathways for physical exercise effects present common elements in skeletal and cardiac muscle, like activation of specific transcription factors, proliferative pathways, and cytokines. More recently, post translational (miRNAs) or epigenetic (DNA methylation) modifications have been demonstrated. However, several points remain unresolved thus requiring new research on the effect of exercise on muscle stem cells.

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Muscle PGC-1α modulates satellite cell number and proliferation by remodeling the stem cell niche

Cited by 32 publications

References 29 publications

Paracrine cross-talk between skeletal muscle and macrophages in exercise by PGC-1α-controlled BNP

Paracrine cross-talk between skeletal muscle and macrophages in exercise by PGC-1α-controlled BNP

The role of AMP‐activated protein kinase in the expression of the dystrophin‐associated protein complex in skeletal muscle

Muscle stem cell and physical activity: what point is the debate at?

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