Serum miRNAs miR-23a, 206, and 499 as Potential Biomarkers for Skeletal Muscle Atrophy.

Fei Wang,Shengju Chen,Jian He,Jinglong Li,Xiaoping Chen,Hongju Liu,Peng Zhang,Wenjiong Li,Jing Wang

doi:10.1155/2017/8361237

Fei Wang, Shengju Chen + Show 7 more

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https://doi.org/10.1155/2017/8361237

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Abstract

Muscle biopsy has long been expected to be replaced by noninvasive biomarkers with diagnostic value and prognostic applications for muscle atrophy. Growing evidence suggests that circulating microRNAs (miRNAs) could act as biomarkers for numerous pathophysiological statuses. In the present study, our results showed that the serum levels of six muscle-specific miRNAs (miR-1/23a/133/206/208b/499) were all elevated in unloading induced mice. The medium levels of these six muscle-specific miRNAs were all elevated in starvation induced atrophic C2C12 myotubes. Moreover, the serum levels of miR-23a/206/499 were induced in participants after 45 days of head-down bed rest (HDBR). The levels of miR-23a/206/499 were positively correlated with the ratio of soleus volume loss in HDBR participants, indicating that they might represent the process of muscle loss. In conclusion, our results demonstrated that circulating miRNAs could serve as useful biochemical and molecular indicators for muscle atrophy diagnosis and disease progression.

Highlights

Muscle atrophy is a common physiological and pathological process, which occurs in response to fasting, chronic disease, and disuse [1,2,3]
Increased protein degradation leads to muscle atrophy, whereas increased protein synthesis leads to muscle hypertrophy
To further evaluate hindlimb unloading (HU)-induced atrophy, frozen sections of soleus muscle from the control and unloaded mice were immunostained with antilaminin (Figure 1(e))

Summary

Introduction

Muscle atrophy is a common physiological and pathological process, which occurs in response to fasting, chronic disease (e.g., cancer, diabetes, AIDS, sepsis, and sarcopenia), and disuse (e.g., long time bed rest and space flight) [1,2,3]. Skeletal muscle possesses high plasticity controlled by a dynamic balance between protein synthesis and degradation. Increased protein degradation leads to muscle atrophy, whereas increased protein synthesis leads to muscle hypertrophy. Muscle atrophy, induced by increased protein degradation and decreased protein synthesis, leads to the deterioration of disease and reduces the quality of life [4, 5]. The diagnosis and treatment of skeletal muscle atrophy is an important clinical issue. Many measurement methods were developed to detect skeletal muscle atrophy, including tomography, magnetic resonance imaging (MRI), and dual-energy X-ray absorptiometry [6]

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