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.