MiR-152 Regulates Bovine Myoblast Proliferation by Targeting KLF6.

Chengchuang Song,Chunlei Zhang,Junhao Chen,Yaqi Chen,Xingtang Fang,Fantong Meng,Lihong Gu,Qi Wang,Zhaoxin Yang,Bei Zhao,Xue Fang,Yanhong Wang

doi:10.3390/ani11103001

Abstract

Simple SummaryOur study found that miR-152 functions in bovine myoblasts to inhibit proliferation. Our prediction and experimental verification revealed that Kruppel-Like Factor 6 (KLF6) is a direct target gene of miR-152. Therefore, miR-152 and its target gene KLF6 have certain effects on the development of bovine skeletal muscles.Though miRNAs have been reported to regulate bovine myoblast proliferation, but many miRNAs still need to be further explored. Specifically, miR-152 is a highly expressed miRNA in cattle skeletal muscle tissues, but its function in skeletal muscle development is unknown. Herein, we aimed to investigate the role of miR-152 in regulating bovine myoblast proliferation. Functionally, RT-qPCR, Western blotting, EdU assay, and flow cytometry detection results showed that miR-152 inhibited bovine myoblast proliferation. Mechanistically, we demonstrated transcription factor KLF6 was a target gene of miR-152 by means of bioinformatics software prediction and dual-luciferase report analysis, which had been demonstrated to be favorable for myoblast proliferation. Collectively, our research suggested that miR-152 inhibits bovine myoblast proliferation via targeting KLF6.

Highlights

Skeletal muscle development is a complex multistage process, which is directed initially from pluripotent stem cells to myogenic progenitor cells and to mononuclear myoblasts [1,2]
After a series of experiments, we demonstrated that miR-152 inhibits bovine myoblast proliferation by targeting KLF6, which is an important transcription factor for skeletal muscle development
The purpose of our experiment was to investigate the role of miR-152 in bovine muscle cell proliferation

Summary

Introduction

Skeletal muscle development is a complex multistage process, which is directed initially from pluripotent stem cells to myogenic progenitor cells and to mononuclear myoblasts [1,2]. Mononuclear myoblasts further proliferate and fuse to form multinucleated myotubes, which fuse to form muscle fibers, and develop into skeletal muscles with the contraction function. The number of muscle fibers generally does not increase anymore [3]. It is of great significance to study the regulatory mechanism of myoblast proliferation. This process could be regulated by positive cell cycle regulators Proliferating cell nuclear antigen (PCNA) [4], cyclin-dependent kinases (CDK2) [5] and cyclin members. Some non-coding RNAs like microRNAs (miRNAs) directly or indirectly regulate the expression of these genes, thereby affecting myoblast proliferation [6,7,8]

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