Expression of microRNA-29b2-c Cluster is Positively Regulated by MyoD in L6 Cells

Liu, Changzheng; Li, Jingjing; Su, Jinmei; Jiao, Tao; Gou, Lijuan; He, Xiaodong; Chang, Yongsheng

doi:10.1016/s1001-9294(13)60039-5

Cited by 3 publications

(2 citation statements)

References 20 publications

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“…Overexpression of myoD resulted in a significant increase in mir-29b levels in L6 cells. Although it has not been verified in vivo [ 32 ], these results corroborate our hypothesis that Myod1 may act as a potential regulator of muscle myogenesis by regulating mir-29b expression. RELA protooncogene (Rela), a component of the NF-kappa B complex, and nuclear factor kappa B subunit 1 (Nfkb1) jointly constitute a transcriptionally active NF-kappa B dimer, which participates in the expression of genes in the processes of immunity, inflammation, and apoptosis [ 33 ].…”

Section: Discussionsupporting

confidence: 89%

Identification of Potential miRNA-mRNA Regulatory Network in Denervated Muscular Atrophy by Bioinformatic Analysis

Wang

Liu

Zhang

et al. 2022

BioMed Research International

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Muscle atrophy caused by long-term denervation leads to the loss of skeletal muscle mass and strength, resulting in a poor recovery of functional muscles and decreasing quality of life. Increasing differentially expressed microRNAs (DEMs) have been reported to be involved in the pathogenesis of denervated muscle atrophy. However, there is still insufficient evidence to explain the role of miRNAs and their target genes in skeletal muscle atrophy. Therefore, an integrative exploration of the miRNA-mRNA regulatory network in denervated muscle atrophy is necessary. A total of 21 (16 upregulated and 5 downregulated) DEMs were screened out in the GSE81914 dataset. Med1, Myod1, Nfkb1, Rela, and Camta1 were predicted and verified to be significantly upregulated in denervated muscle atrophy, from which 6 key TF-miRNA relationship pairs, including Med1-mir-1949, Med1-mir-146b, Myod1-mir-29b, Nfkb1-mir-21, Rela-mir-21, and Camta1-mir-132, were obtained. 60 target genes were then predicted by submitting candidate DEMs to the miRNet database. GO and KEGG pathway enrichment analysis showed that target genes of DEMs were mainly enriched in the apoptotic process and PI3K/Akt signaling pathway. Through the PPI network construction, key modules and hub genes were obtained and potentially modulated by mir-29b, mir-132, and mir-133a. According to the qRT-PCR results, the expression of COL1A1 and Ctgf is opposite to their related miRNAs in denervated muscle atrophy. In the study, a potential miRNA-mRNA regulatory network was firstly constructed in denervated muscle atrophy, in which the mir-29b-COL1A1 and mir-133a-Ctgf pathways may provide new insights into the pathogenesis and treatment.

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Section: Discussionsupporting

confidence: 89%

Identification of Potential miRNA-mRNA Regulatory Network in Denervated Muscular Atrophy by Bioinformatic Analysis

Wang

Liu

Zhang

et al. 2022

BioMed Research International

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“…In skeletal muscle, highly expressed miRNAs are called myomiRs, which include miR-1, miR-133a, miR-133b, miR-206, miR-208a, miR-208b, miR-486 and miR-499 [ 23 ]. Besides the myomiRs, there are also many miRNAs regulating satellite cell myogenesis, for example miR-31 [ 24 ]; miR-27a [ 25 , 26 ], miR128 [ 27 ], miR-221/miR-222 [ 28 ], miR-682 [ 29 ] and miR-181 [ 30 ]; miR-186 [ 31 ], miR-24 [ 32 ], miR-214 [ 33 , 34 ], miR-26a [ 35 ], miR-29b/c [ 36 ], miR-322/424 [ 37 ] and miR-503 [ 37 ] have been identified to regulate the quiescence, proliferation and differentiation stage of satellite cells respectively. Both Notch signaling and miRNA have been identified to play critical roles in regulating myogenesis, and four miRNAs, miR-1, miR-206, miR-146a and 146b, have been reported to regulate skeletal muscle myogenesis via Notch signaling [ 38 , 39 , 40 , 41 ].…”

Section: Introductionmentioning

confidence: 99%

Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells’ Proliferation through Regulating the Cell Cycle

Jiao

Huang

Chen

et al. 2018

IJMS

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Notch signaling as a conserved cell fate regulator is involved in the regulation of cell quiescence, proliferation, differentiation and postnatal tissue regeneration. However, how Notch signaling regulates porcine satellite cells (PSCs) has not been elucidated. We stably transfected Notch1 intracellular domain (N1ICD) into PSCs to analyze the gene expression profile and miRNA-seq. The analysis of the gene expression profile identified 295 differentially-expressed genes (DEGs) in proliferating-N1ICD PSCs (P-N1ICD) and nine DEGs on differentiating-N1ICD PSCs (D-N1ICD), compared with that in control groups (P-Control and D-Control, respectively). Analyzing the underlying function of DEGs showed that most of the upregulated DEGs enriched in P-N1ICD PSCs are related to the cell cycle. Forty-four and 12 known differentially-expressed miRNAs (DEMs) were identified in the P-N1ICD PSCs and D-N1ICD PSCs group, respectively. Furthermore, we constructed the gene-miRNA network of the DEGs and DEMs. In P-N1ICD PSCs, miR-125a, miR-125b, miR-10a-5p, ssc-miR-214, miR-423 and miR-149 are downregulated hub miRNAs, whose corresponding hub genes are marker of proliferation Ki-67 (MKI67) and nuclear receptor binding SET domain protein 2 (WHSC1). By contrast, miR-27a, miR-146a-5p and miR-221-3p are upregulated hub miRNAs, whose hub genes are RUNX1 translocation partner 1 (RUNX1T1) and fibroblast growth factor 2 (FGF2). All the hub miRNAs and genes are associated with cell proliferation. Quantitative RT-PCR results are consistent with the gene expression profile and miRNA-seq results. The results of our study provide valuable information for understanding the molecular mechanisms underlying Notch signaling in PSCs and skeletal muscle development.

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Exenatide reverses dysregulated microRNAs in high-fat diet-induced obese mice

Lee

Park

Yang

et al. 2016

Obesity Research & Clinical Practice

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Expression of microRNA-29b2-c Cluster is Positively Regulated by MyoD in L6 Cells

Abstract: MyoD might act as a crucial regulator of myogenesis and glucose metabolism in muscle through regulating the expression of miR-29b2-c.

Cited by 3 publications

References 20 publications

Identification of Potential miRNA-mRNA Regulatory Network in Denervated Muscular Atrophy by Bioinformatic Analysis

Identification of Potential miRNA-mRNA Regulatory Network in Denervated Muscular Atrophy by Bioinformatic Analysis

Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells’ Proliferation through Regulating the Cell Cycle

Exenatide reverses dysregulated microRNAs in high-fat diet-induced obese mice

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