Abstract
Akirin1 is found to be involved in myoblast differentiation. However, the mechanism by which the Akirin1 gene regulates myoblast differentiation still remains unclear. In the present study, we found that ectopic expression of Akirin1 promoted myoblast differentiation by increasing the expression of myogenic regulatory factor (MRF) 4 (MRF4) and myocyte enhancer factor 2B (MEF2B) mRNA. Additionally, we showed that ectopic Akirin1 induced cell cycle arrest by up-regulating p21 mRNA. To further uncover the mechanism by which Akirin1 promotes myoblast differentiation, we showed that the enhanced Akirin1 increased the mRNA expression of P38α. Importantly, the enhanced MRF4 expression by Akirin1 can be abrogated by treatment of SB203580, a p38 inhibitor. Similarly, we found that enhanced MEF2B expression by Akirin1 can be abrogated by treatment with LY294002, a PI3K inhibitor. Together, our results indicate that Akirin1 promotes myoblast differentiation by acting on the p38 and PI3K pathways and subsequently inducing the expression of myoblast differentiation factors.
Highlights
We showed that the expression of MEF2A and MEF2C irregularly increased to a high level and decreased (Figure 4A,C), while the expression of myocyte enhancer factor 2B (MEF2B) and MEF2D progressively increased to a high level (Figure 4B,D)
Myoblast differentiation is a highly ordered process that is initially induced by several myogenic regulatory factor (MRF) [22]
We found that ectopic expression of Akirin1 significantly increased the mRNA expression of MyoG at 12 h, and significantly increased the mRNA expression of MRF4 which plays a critical role in initiating myoblast differentiation as well [23]
Summary
Myoblast differentiation initiated by the expression of the MRFs (myogenic regulatory factors), such as Myf, MyoD, MyoG, and MRF4 [2,3,4]. Myf and MyoD are mainly involved in muscle specification and trigger conversion of non-muscle cells [5,6], whereas MyoG and MRF4 act later during myogenesis and allow myotube formation and maturation [3,7]. This conversion ability is greatly enhanced when MRFs are co-transfected with MEF2s (myocyte enhancer factors 2s) (MEF2A–D) [8]. A tight regulation of differentiation is critical for the production of functional muscle
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