Effects of microRNAs on skeletal muscle development

Wang, J.; Yang, Lingzhi; Zhang, J.S.; Gong, Junhua; Wang, Y.H.; Zhang, C.L.; Chen, H.; Fang, Xingtang

doi:10.1016/j.gene.2018.05.039

Cited by 54 publications

(51 citation statements)

References 57 publications

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“…The development of skeletal muscle is a complex process, and understanding the details of the myogenesis is very important . Many studies have shown that miRNAs play a vital role in myogenesis . The specific miRNA in skeletal muscle also regulates the proliferation and differentiation of myoblasts.…”

Section: Discussionmentioning

confidence: 99%

“…[35][36][37] Many studies have shown that miRNAs play a vital role in myogenesis. [38][39][40] The specific miRNA in skeletal muscle also regulates the proliferation and differentiation of myoblasts. An analysis of the miRNAs in longissimus dorsi of Rongchang pig revealed that miR-323-3p had significant expression changes in different age groups.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐323‐3p promotes myogenesis by targeting Smad2

Qin

Sun

Liu

et al. 2019

J of Cellular Biochemistry

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Skeletal muscle is an important and complex organ with multiple biological functions in humans and animals. Proliferation and differentiation of myoblasts are the key steps during the development of skeletal muscle. MicroRNA (miRNA) is a class of 21‐nucleotide noncoding RNAs regulating gene expression by combining with the 3′‐untranslated region of target messenger RNA. Many studies in recent years have suggested that miRNAs play a critical role in myogenesis. Through high‐throughput sequencing, we found that miR‐323‐3p showed significant changes in the longissimus dorsi muscle of Rongchang pigs in different age groups. In this study, we discovered that overexpression of miR‐323‐3p repressed myoblast proliferation and promoted differentiation, whereas the inhibitor of miR‐323‐3p displayed the opposite results. Furthermore, we predicted Smad2 as the target gene of miR‐323‐3p and found that miR‐323‐3p directly modulated the expression level of Smad2. Then luciferase reporter assays verified that Smad2 was a target gene of miR‐323‐3p during the differentiation of myoblasts. These findings reveal that miR‐323‐3p is a positive regulator of myogenesis by targeting Smad2. This provides a novel mechanism of miRNAs in myogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA‐323‐3p promotes myogenesis by targeting Smad2

Qin

Sun

Liu

et al. 2019

J of Cellular Biochemistry

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“…MiR-1, miR-133a, miR-133b, and miR-206 are designed as canonical myomiRs and they are predominantly expressed in cardiac and skeletal muscle [33]. MyomiRs take part in the molecular network regulating myogenesis, muscle development, repair, and remodeling [34,35]. MiRNA-1 and -206 share specific targets that are closely related to functioning: both promote myoblast differentiation in myotubes and cell proliferation [33,36].…”

Section: Discussionmentioning

confidence: 99%

Myomirnas Role in Als Suggest a Crosstalk between Muscle and Motor Neuron

Pegoraro¹,

Merico²,

Angelini³

2018

Preprint

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Amyotrophic lateral sclerosis (ALS) is a rare, progressive, neurodegenerative disorder caused by degeneration of upper and lower motor neurons. The disease process leads from lower motor neuron involvement to progressive muscle atrophy, weakness, fasciculations for the upper motor neuron involvement to spasticity. Muscle atrophy in ALS is caused by a dysregulation in the molecular network controlling fast and slow muscle fibres. Denervation and reinnervation processes in skeletal muscle occur in the course of ALS and are modulated by rehabilitation. MicroRNAs (miRNAs) are small non-coding RNAs that modulate a wide range of biological functions under various pathophysiological conditions. MiRNAs can be secreted by various cell types and they are markedly stable in body fluids. MiR-1, miR-133 a, miR-133b, and miR-206 are called “myomiRs” and are considered markers of myogenesis during muscle regeneration and neuromuscular junction stabilization or sprouting. We observed a positive effect of a standard aerobic exercise rehabilitative protocol conducted for six weeks in 18 ALS patients during hospitalization in our center. We correlated clinical scales with molecular data on myomiRs. After six weeks of moderate aerobic exercise, myomiRNAs were down-regulated, suggesting an active proliferation of satellite cells in muscle and increased neuromuscular junctions. Our data suggest that circulating miRNAs modulate during skeletal muscle recovery in response to physical rehabilitation in ALS.

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“…It is well known that miRNAs lead to post-transcriptional silencing of their target mRNAs through complementary binding to the 3 untranslated region (UTR) of mRNA targets. Previous studies have suggested that miRNAs are required for skeletal development using mice with conditional knockdown of Dicer in chondrocytes of the growth plate [4,5]. Accumulating evidence indicates that miRNAs play an important role in regulating multiple developmental processes in diverse organisms such as stem cell chondrogenic differentiation for osteogenic differentiation or articular cartilage regeneration [6].…”

Section: Introductionmentioning

confidence: 99%

MiR-132/212 promotes the growth of precartilaginous stem cells (PCSCs) by regulating Ihh/PTHrP signaling pathway

et al. 2020

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Precartilaginous stem cells (PCSCs) are adult stem cells that can initiate chondrocytes and bone development. In the present study, we explored whether miR-132/212 was involved in the proliferation of PCSCs via Hedgehog signaling pathway. PCSCs were isolated and purified with the fibroblast growth factor receptor-3 (FGFR-3) antibody. Cell viability, DNA synthesis and apoptosis were measured using MTT, BrdU and flow cytometric analysis. The mRNA and protein expression were detected by real-time PCR and Western blot, respectively. The target gene for miR-132/212 was validated by luciferase reporter assay. Results showed that transfection with miR-132/212 mimic significantly increased cell viability and DNA synthesis, and inhibited apoptosis of PCSCs. By contrast, miR-132/212 inhibitor could suppress growth and promote apoptosis of PCSCs. Luciferase reporter assays indicated that transfection of miR-132/212 led to a marked reduction of luciferase activity, but had no effect on PTCH1 3′-UTR mutated fragment, suggesting that Patched1 (PTCH1) is a target of miR-132/212. Furthermore, treatment with miR-132/212 mimics obviously increased the protein expression of Indian hedgehog (Ihh) and parathyroid hormone related protein (PTHrP), which was decreased after treatment with Hedgehog signaling inhibitor, cyclopamine. We also found that inhibition of Ihh/PTHrP signaling by cyclopamine significantly suppressed growth and DNA synthesis, and induced apoptosis in PCSCs. These findings demonstrate that miR-132/212 promotes growth and inhibits apoptosis in PCSCs by regulating PTCH1-mediated Ihh/PTHrP pathway, suggesting that miR-132/212 cluster might serve as a novel target for bone diseases.

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Effects of microRNAs on skeletal muscle development

Cited by 54 publications

References 57 publications

MicroRNA‐323‐3p promotes myogenesis by targeting Smad2

MicroRNA‐323‐3p promotes myogenesis by targeting Smad2

Myomirnas Role in Als Suggest a Crosstalk between Muscle and Motor Neuron

MiR-132/212 promotes the growth of precartilaginous stem cells (PCSCs) by regulating Ihh/PTHrP signaling pathway

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