This study aimed to assess the effect of the glucocorticoid dexamethasone (Dex) on the differentiation process in an in vitro culture of Phf2 knockout (KO) myoblasts.
C2C12 myoblasts (Ctr) and Phf2 KO C2C12 myoblasts were cultured and treated with Dex. After 7 days of differentiation, the myotubes were subjected to quantitative real-time polymerase chain reaction (PCR) analysis and immunofluorescence staining. Real-time PCR for mRNA analysis was performed using specific primers for MHC-I (Myh7) as the slow type, MHC-IIa (Myh2) as the fast type, and PGC-1α. The diameter of the myotubes, stained with an anti-myosin heavy chain antibody, was measured for each myotube.
The expressions of terminal differentiation genes (Myh7 and Myh2) and Ppargc1a were highly expressed in Ctr and Phf2 KO myotubes treated with Dex. However, the expressions of Myh7 and Myh2 were higher in Ctr compared with Ph2 KO myotubes. The diameter of myotubes increased in Ctr and Phf2 KO myotubes after treatment with Dex.
The results of this study indicated that Dex treatment led to a trend toward the slow-twitch muscle type. Furthermore, Phf2 KO myotubes were less affected by Dex treatment compared to control myotubes. The study also found that the diameter of myotubes increased with Dex treatment. As Dex was administered from day 0, myotube formation may have been inhibited, resulting in more myoblasts fusing to the already-formed myotubes.
This study provides valuable insights for physiotherapists when treating patients with muscle atrophy and selecting appropriate treatments for promoting muscle recovery.
Phf2
differentiation
