Abstract
Skeletal muscle atrophy is a well-known adverse effect of long-term glucocorticoid (GC) therapy. MicroRNAs (miRNAs or miRs) and long non-coding RNAs (lncRNAs) are important regulators in a number of physiological and pathological processes. However, the role of miRNAs and lncRNAs in the regulation of GC-treated muscle atrophy remains poorly understood. In the current study, muscular atrophy was induced and the results indicated that C2C12 myotubes were thinner than normal, while the expression of muscle ring finger protein 1 and Atrogin-1 was increased. The expression of nine miRNAs and seven lncRNAs associated with proliferation and differentiation were analyzed in a dexamethasone (DEX)-induced muscle atrophy cell model. In addition, the mRNA expression of the downstream targets of lncRNAs that were differentially expressed between DEX-treated and control cells were determined. The results indicated that the expression of miR-133a, miR-133b, miR-206 and five lncRNAs (increased Atrolnc-1, Dum, MAR1, linc-MD1 and decreased Myolinc) were significantly different between the DEX and the control group. Furthermore, the relative mRNA expression of Wnt5a and MyoD was significantly different between the two groups. The results of the current study indicated that some important miRNAs and lncRNAs are associated with DEX-induced muscle atrophy and have the potential to be further developed as a diagnostic tool for this condition.
Keywords:
atrophy; dexamethasone; long non-coding RNAs; microRNAs; skeletal muscle cells.