PGC-1α is associated with C2C12 Myoblast differentiation

Abstract

PGC-1α has been implicated as an important mediator of functional capacity of skeletal muscle. However, the role of PGC-1α in myoblast differentiation remains unexplored. In the present study, we observed a significant up-regulation of PGC-1α expression during the differentiation of murine C2C12 myoblast. To understand the biological significance of PGC-1α up-regulation in myoblast differentiation, C2C12 cells were transfected with murine PGC-1α cDNA and siRNA targeting PGC-1α, respectively. PGC-1α over-expressing clones fused to form typical myotubes with higher mRNA level of myosin heavy chain isoform I (MyHCI) and lower MyHCIIX. No obvious differentiation was observed in PGC-1α-targeted siRNA-transfected cells with marked decrement of mRNA levels of MyHCI and MyHCIIX. Furthermore, PGC-1α increased the expression of MyoD and MyoG in C2C12 cells, which controlled the commitment of precursor cells to myotubes. These results indicate that PGC-1α is associated with myoblast differentiation and elevates MyoD and MyoG expression levels in C2C12 cells.

PGC-1α is associated with Schizothorax prenanti myoblast differentiation

“…While the decreased constitutive expression of PGC-1α via transfection of shRNA-targeting PGC-1α leaded to no obvious myotube formation. The observation was parallel with our previous report that PGC-1α promoted typical myotube formation in murine C2C12 myoblast (Lin et al, 2014). These results suggested that PGC-1α was associated with myoblast differentiation.…”

Combined speed endurance and endurance exercise amplify the exercise‐induced PGC‐1α and PDK4 mRNA response in trained human muscle

“…MRF4 is part of the myogenic regulatory factor family that drive muscle gene expression during myogenesis (Singh and Dilworth 2013) and the level of muscle MRF4 mRNA can increase as a response to both resistance and endurance exercise in untrained (Psilander et al 2003) and trained subjects (Yang et al 2005;Harber et al 2009). The present finding that only combined speed endurance and endurance exercise induced increased muscle MRF4 mRNA level may be caused by the upregulation of muscle PGC-1a mRNA, as PGC-1a has been shown to be associated with accelerated myoblast differentiation (Lin et al 2014 mitochondrial biogenesis, the crosstalk between PGC-1a and myoblast differentiation, may coordinate mitochondrial regulation. However, the observation that no change occurred in muscle MRF4 mRNA although the PGC-1a mRNA level increased with single-mode speed endurance exercise does not support this, and studies are needed to explore this possible relationship.…”

“…The present finding that only combined speed endurance and endurance exercise induced increased muscle MRF4 mRNA level may be caused by the upregulation of muscle PGC‐1 α mRNA, as PGC‐1 α has been shown to be associated with accelerated myoblast differentiation (Lin et al. ). Thus, it could be speculated that because PGC‐1 α is a master regulator of mitochondrial biogenesis, the crosstalk between PGC‐1 α and myoblast differentiation, may coordinate mitochondrial regulation.…”

Neuropeptide Y damages the integrity of mitochondrial structure and disrupts energy metabolism in cultured neonatal rat cardiomyocytes

“…Recent results point to a central role for the PGC-1␣ in integrating mitochondrial biogenesis and energy production with many diverse cellular functions. One laboratory has reported that the levels of PGC-1␣ mRNA were decreased in myogenic differentiation [21]. Another report proved NPY compromised the effect of db-cAMP on stimulating mRNA expression of PGC-1␣ in brown-like adipocytes [34].…”