MicroRNA-133 modulates skeletal muscle hypertrophy through regulating JunB
Date Issued
2014
Date
2014
Author(s)
Chang, Chiao-Yi
Abstract
MicroRNAs (miRNAs) are short non-coding RNA molecules that post-transcriptionally inhibit gene expression. Muscle specific miRNAs, myomiRs, have been shown to play an essential role in regulating muscle development and growth. A previous study showed that downregulated miR-1 and miR-133 expression results in skeletal muscle hypertrophy after functional overload. However, the muscle hypertrophy regulatory roles of miRNAs are still unclear. It has been known that muscle mass is regulated by the balance between the synthesis and degradation of proteins in myofibers. Intracellular protein synthesis is mainly regulated by the activation of IGF-1/-Akt/-mammalian target of rapamycin (mTOR) pathway. The AP-1 transcription factor JunB is another efficient factor that induces rapid adult muscle hypertrophy without affecting satellite cell activation and Akt/mTOR pathway by inhibiting the downstream atrophy-related genes, Atrogin-1 and MuRF-1 expression. Our research utilized a bioinformatic software to predict the miRNA binding sites of target genes and has identified a putative miR-133 binding site on the 3’UTR of JunB in humans and zebrafish. Here we identify JunB as one of the direct regulatory targets of miR-133 by a luciferase assay, real-time PCR, and western blot in vitro. The JunB mRNA rescue assay successfully reversed the miR-133-induced muscle atrophy in zebrafish larvae. miR-133 modulates skeletal muscle hypertrophy by regulatiing JunB translation in zebrafish. The novel mechanism may pave the way for new therapies for disease-induced muscle atrophy.
Subjects
斑馬魚
骨骼肌肥大
微核糖核酸-133
JunB
Atrogin-1
MuRF-1
SDGs
Type
thesis
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