Abstract
Skeletal muscle is a highly plastic organ that is necessary for homeostasis and health of the human body. The size of skeletal muscle changes in response to intrinsic and extrinsic stimuli. Although protein-coding RNAs including myostatin, NF-κβ, and insulin-like growth factor-1 (IGF-1), have pivotal roles in determining the skeletal muscle mass, the role of long non-coding RNAs (lncRNAs) in the regulation of skeletal muscle mass remains to be elucidated. Here, we performed expression profiling of nine skeletal muscle differentiation-related lncRNAs (DRR, DUM1, linc-MD1, linc-YY1, LncMyod, Neat1, Myoparr, Malat1, and SRA) and three genomic imprinting-related lncRNAs (Gtl2, H19, and IG-DMR) in mouse skeletal muscle. The expression levels of these lncRNAs were examined by quantitative RT-PCR in six skeletal muscle atrophy models (denervation, casting, tail suspension, dexamethasone-administration, cancer cachexia, and fasting) and two skeletal muscle hypertrophy models (mechanical overload and deficiency of the myostatin gene). Cluster analyses of these lncRNA expression levels were successfully used to categorize the muscle atrophy models into two sub-groups. In addition, the expression of Gtl2, IG-DMR, and DUM1 was altered along with changes in the skeletal muscle size. The overview of the expression levels of lncRNAs in multiple muscle atrophy and hypertrophy models provides a novel insight into the role of lncRNAs in determining the skeletal muscle mass.
Highlights
Skeletal muscle is an organ that plays important roles in motion, postural maintenance, and metabolic adaptation
We examined the expression of nine skeletal muscle differentiation-related long non-coding RNAs (lncRNAs) (Myoparr, linc-MD1, LncMyod, DRR, DUM1, linc-YY1, Malat1, Neat1, and SRA) in six muscle atrophy models in mice
Recent findings indicate that denervation, immobilization, cancer cachexia, chronic kidney disease, fasting, and aging affect the expression of Pvt1, lncMUMA, Atrolnc-1, and MAR1 lncRNAs in the skeletal muscles [48,49,50,51]
Summary
Skeletal muscle is an organ that plays important roles in motion, postural maintenance, and metabolic adaptation. The skeletal muscle mass is decreased in diseases, such as cancer cachexia, neuromuscular disorders, chronic kidney disease, heart failure, and chronic obstructive pulmonary disease, and as a consequence of aging, immobilization, and malnutrition [1,2,3,4,5,6,7,8]. The latter type of loss in the muscle mass is better known as muscle atrophy or wasting condition, which affects the activities of daily living and leads to increased mortality from diseases [9,10]. Understanding the molecular mechanisms controlling skeletal muscle mass is important to extend the healthy life expectancy in humans
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