Related Experiment Video
Updated: Mar 8, 2026

Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents
Published on: August 10, 2018
MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6
Qianru He1, Jiaying Qiu1, Ming Dai2
1Jiangsu Key Laboratory of Neuroregeneration, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Abstract:
MicroRNAs (miRs) have been observed to be involved in the modulation of various physiopathological processes. However, the impacts of miRNAs on muscle atrophy have not been fully investigated. In the present study, the results demonstrated that miR-351 was differentially expressed in the tibialis anterior (TA) muscle at various times following sciatic nerve transection, and the time-dependent expression profile of miR-351 was inversely correlated with that of tumor necrosis factor receptor-associated factor 6 (TRAF6) at the mRNA and protein levels. The dual luciferase reporter assay indicated that miR-351 was able to significantly downregulate the expression levels of TRAF6 by directly targeting the 3'-untranslated region of TRAF6. Overexpression of miR-351 inhibited a significant decrease in the wet weight ratio or cross-sectional area of the TA muscle following sciatic nerve transection. Western blot analysis indicated that the protein expression levels of TRAF6, muscle ring-finger protein 1 (MuRF1) and muscle atrophy F-box (MAFBx) in denervated TA muscles were suppressed by overexpression of miR-351. These results demonstrate that miR-351 inhibits denervation-induced atrophy of TA muscles following sciatic nerve transection at least partially through negative regulation of TRAF6 as well as MuRF1 and MAFBx, the two downstream signaling molecules of TRAF6.
Insights
MicroRNAs (miRs) regulate muscle mass. This study found that miR-351 inhibits muscle atrophy after nerve injury by targeting TRAF6, MuRF1, and MAFBx, preserving muscle size and function.
Area of Science:
- Molecular Biology
- Muscle Physiology
- Biochemistry
Background:
- MicroRNAs (miRs) are implicated in various physiological and pathological processes.
- The role of miRs in muscle atrophy, particularly following nerve injury, remains incompletely understood.
Purpose of the Study:
- To investigate the role of miR-351 in denervation-induced muscle atrophy.
- To identify the molecular targets and mechanisms through which miR-351 modulates muscle atrophy.
Main Methods:
- Sciatic nerve transection model in tibialis anterior (TA) muscle.
- Quantitative real-time PCR and Western blot analysis for gene and protein expression.
- Dual luciferase reporter assay to confirm direct targeting.
- Assessment of muscle weight and cross-sectional area.
Main Results:
- miR-351 expression was inversely correlated with TRAF6 (Tumor Necrosis Factor Receptor-Associated Factor 6) mRNA and protein levels post-nerve injury.
- miR-351 directly targeted the 3'-untranslated region of TRAF6, downregulating its expression.
- Overexpression of miR-351 attenuated denervation-induced reductions in TA muscle weight and cross-sectional area.
- miR-351 overexpression suppressed the protein levels of TRAF6, MuRF1 (Muscle Ring-Finger Protein 1), and MAFBx (Muscle Atrophy F-box) in denervated muscle.
Conclusions:
- miR-351 plays a protective role against denervation-induced muscle atrophy in the tibialis anterior muscle.
- This protective effect is mediated, at least partly, by the negative regulation of TRAF6 and its downstream targets, MuRF1 and MAFBx.
Related Concept Videos
MicroRNAs
MicroRNAs
Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin
The binding of dantrolene to the RYR1...

