Let-7e-5p Regulates IGF2BP2, and Induces Muscle Atrophy

Overview

Journal Front Endocrinol (Lausanne)

Specialty Endocrinology

Date 2022 Jan 10

PMID 35002969

Authors

Takuro Okamura

Hiroshi Okada

Yoshitaka Hashimoto

Saori Majima

Takafumi Senmaru

Naoko Nakanishi

Mai Asano

Masahiro Yamazaki

Masahide Hamaguchi

Michiaki Fukui

Affiliations

Soon will be listed here.

Abstract

Background And Aims: To understand the role of microRNAs in muscle atrophy caused by androgen-depletion, we performed microarray analysis of microRNA expression in the skeletal muscles of Sham, orchiectomized (ORX), and androgen-treated ORX mice.

Methods: To clarify role and mechanisms of let-7e-5p in the muscle, the effect of let-7e-5p overexpression or knockdown on the expression of myosin heavy chain, glucose uptake, and mitochondrial function was investigated in C2C12 myotube cells. Moreover, we examined serum let-7e-5p levels among male subjects with type 2 diabetes.

Results: We found that the expression of the miRNA, lethal was significantly lower in ORX mice than that in Sham mice (p = 0.027); however, expression in androgen-treated ORX mice was higher (p = 0.047). Suppression of let-7e-5p significantly upregulated the expression of myosin heavy chain, glucose uptake, and mitochondrial function. Real-time PCR revealed a possible regulation involving let-7e-5p and mRNA and protein in C2C12 cells. The serum let-7e-5p levels were significantly lower, which might be in compensation, in subjects with decreased muscle mass compared to subjects without decreased muscle mass. Let-7e-5p downregulates the expression of in myotube cells and inhibits the growth of the myosin heavy chain.

Conclusions: Based on our study, serum level of let-7e-5p may be used as a potential diagnostic marker for muscle atrophy.

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