miR‐122‐5p negatively regulates the transforming growth factor‐β/Smad signaling pathway in skeletal muscle myogenesis

Ding, Zheci; Lin, Jinrong; Sun, Yaying; Cong, Shuang; Liu, Shaohua; Zhang, Yuhan; Chen, Qingyan; Chen, Jiwu

doi:10.1002/cbf.3460

Cited by 14 publications

(15 citation statements)

References 46 publications

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“…The TGFB signaling starts with the binding of the ligand to type 1 and 2 membrane receptors, forcing their assembly into a complex that initiates the phosphorylation cascade [99]. In this sense, the activation of tgfbr2 was associated with myod and myog down-regulation in C2C12 cells, and the tgfbr2 inhibition by miRNA resulted in a reversed effect [100]. In addition, Accornero et al (2014) showed that the blocking of TGFB signaling through TGFBR2 mutant attenuated muscular dystrophy and injury, and improved muscle regeneration and satellite cell numbers in mice [101], indicating a negative regulation by tgfbr2 in muscle growth.…”

Section: Discussionmentioning

confidence: 99%

Amino Acids and IGF1 Regulation of Fish Muscle Growth Revealed by Transcriptome and microRNAome Integrative Analyses of Pacu (Piaractus mesopotamicus) Myotubes

Duran

Zanella

Perez

et al. 2022

IJMS

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Amino acids (AA) and IGF1 have been demonstrated to play essential roles in protein synthesis and fish muscle growth. The myoblast cell culture is useful for studying muscle regulation, and omics data have contributed enormously to understanding its molecular biology. However, to our knowledge, no study has performed the large-scale sequencing of fish-cultured muscle cells stimulated with pro-growth signals. In this work, we obtained the transcriptome and microRNAome of pacu (Piaractus mesopotamicus)-cultured myotubes treated with AA or IGF1. We identified 1228 and 534 genes differentially expressed by AA and IGF1. An enrichment analysis showed that AA treatment induced chromosomal changes, mitosis, and muscle differentiation, while IGF1 modulated IGF/PI3K signaling, metabolic alteration, and matrix structure. In addition, potential molecular markers were similarly modulated by both treatments. Muscle-miRNAs (miR-1, -133, -206 and -499) were up-regulated, especially in AA samples, and we identified molecular networks with omics integration. Two pairs of genes and miRNAs demonstrated a high-level relationship, and involvement in myogenesis and muscle growth: marcksb and miR-29b in AA, and mmp14b and miR-338-5p in IGF1. Our work helps to elucidate fish muscle physiology and metabolism, highlights potential molecular markers, and creates a perspective for improvements in aquaculture and in in vitro meat production.

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Section: Discussionmentioning

confidence: 99%

Amino Acids and IGF1 Regulation of Fish Muscle Growth Revealed by Transcriptome and microRNAome Integrative Analyses of Pacu (Piaractus mesopotamicus) Myotubes

Duran

Zanella

Perez

et al. 2022

IJMS

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“…The downregulation of miR-122-5p has been found in skeletal muscle fibrosis, and miR-122-5p overexpression has been shown to retard the fibrotic process by targeting the TGF-β/Smad signaling pathway [ 23 ]. Another study showed a similar result: miR-122-5p may restore myogenesis [ 24 ]. These combined results show the potential therapeutic effects of this miRNA in translational studies.…”

Section: Discussionmentioning

confidence: 73%

Altered expression of microRNAs in the rat diaphragm in a model of ventilator-induced diaphragm dysfunction after controlled mechanical ventilation

Wang

Zhou

et al. 2021

BMC Genomics

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Background Ventilator-induced diaphragm dysfunction (VIDD) is a common complication of life support by mechanical ventilation observed in critical patients in clinical practice and may predispose patients to severe complications such as ventilator-associated pneumonia or ventilator discontinuation failure. To date, the alterations in microRNA (miRNA) expression in the rat diaphragm in a VIDD model have not been elucidated. This study was designed to identify these alterations in expression. Results Adult male Wistar rats received conventional controlled mechanical ventilation (CMV) or breathed spontaneously for 12 h. Then, their diaphragm tissues were collected for RNA extraction. The miRNA expression alterations in diaphragm tissue were investigated by high-throughput microRNA-sequencing (miRNA-seq). For targeted mRNA functional analysis, gene ontology (GO) analyses and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were subsequently conducted. qRT-PCR validation and luciferase reporter assays were performed. We successfully constructed a model of ventilator-induced diaphragm dysfunction and identified 38 significantly differentially expressed (DE) miRNAs, among which 22 miRNAs were upregulated and 16 were downregulated. GO analyses identified functional genes, and KEGG pathway analyses revealed the signaling pathways that were most highly correlated, which were the MAPK pathway, FoxO pathway and Autophagy–animal. Luciferase reporter assays showed that STAT3 was a direct target of both miR-92a-1-5p and miR-874-3p and that Trim63 was a direct target of miR-3571. Conclusions The current research supplied novel perspectives on miRNAs in the diaphragm, which may not only be implicated in diaphragm dysfunction pathogenesis but could also be considered as therapeutic targets in diaphragm dysfunction.

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“…Several studies have demonstrated that miR-122-5p participates in the development of various diseases ( 19 , 20 , 33 ). Ma et al ( 33 ) revealed that miR-122-5p inhibited osteosarcoma cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…Ma et al ( 33 ) revealed that miR-122-5p inhibited osteosarcoma cell proliferation. Ding et al ( 19 ) demonstrated that miR-122-5p promoted skeletal muscle myogenesis via transforming growth factor β receptor 2. Yang et al ( 20 ) demonstrated that miR-122-5p downregulation can protect against acetaminophen-mediated liver damage by upregulating NDRG family member 3 expression.…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs do not encode proteins, but instead inhibit target gene expression (15)(16)(17). miR-122-5p is located at chr18q21.31, and it has been demonstrated to participate in the development of several diseases, including cancer (18), skeletal muscle myogenesis (19), drug-induced liver injury (20) and radiation-induced rectal injury (21). In addition, Lu et al (22) revealed that miR-122-5p was involved in ALI development; miR-122-5p expression in ALI was notably upregulated, and it was demonstrated to regulate pulmonary microvascular endothelial cells by affecting the dual specificity phosphatase 4 (DUSP4)/ERK signaling pathway to aggravate ALI (22).…”

Section: Introductionmentioning

confidence: 99%

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miR‑122‑5p downregulation attenuates lipopolysaccharide‑induced acute lung injury by targeting IL1RN

Zeng

Wang

2021

Exp Ther Med

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MicroRNAs (miRs) and inflammatory cytokines can induce acute lung injury (ALI), which can develop into acute respiratory distress syndrome in severe cases. Previous research has revealed that miR-122-5p participates in the development of ALI, and that its expression is positively associated with ALI. However, the mechanism by which miR-122-5p contributes to ALI remains to be determined. In the current study, TargetScan and dual luciferase reporter gene assays were used to confirm that IL-1 receptor antagonist (IL1RN) was a target of miR-122-5p. Subsequently, by referring to previous literature, a lipopolysaccharide (LPS)-induced ALI cell model was established. A549 cells were transfected with mimic control or miR-122-5p mimics for 24 h, and 10 µg LPS was used to treat the transfected cells for 12 h. The results revealed that miR-122-5p mimics decreased cell viability and promoted apoptosis. Lactate dehydrogenase (LDH) release assays indicated that miR-122-5p mimics increased LDH release. ELISA demonstrated that miR-122-5p mimics promoted TNF-α, IL-1β and IL-6 expression levels. A549 cells were transfected with inhibitor control, miR-122-5p inhibitor, miR-122-5p inhibitor + control-small interfering (si)RNA or miR-122-5p inhibitor + IL1RN-siRNA for 24 h, after which the cells were treated with 10 µg LPS for 12 h. The results revealed that the effects of the miR-122-5p inhibitor were the opposite of those of the miR-122-5p mimic. All the effects of miR-122-5p inhibitor on LPS-treated A549 cells were significantly reversed by IL1RN-siRNA. Overall, the results highlighted miR-122-5p as a potential novel target for the treatment of ALI.

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miR‐122‐5p negatively regulates the transforming growth factor‐β/Smad signaling pathway in skeletal muscle myogenesis

Cited by 14 publications

References 46 publications

Amino Acids and IGF1 Regulation of Fish Muscle Growth Revealed by Transcriptome and microRNAome Integrative Analyses of Pacu (Piaractus mesopotamicus) Myotubes

Amino Acids and IGF1 Regulation of Fish Muscle Growth Revealed by Transcriptome and microRNAome Integrative Analyses of Pacu (Piaractus mesopotamicus) Myotubes

Altered expression of microRNAs in the rat diaphragm in a model of ventilator-induced diaphragm dysfunction after controlled mechanical ventilation

miR‑122‑5p downregulation attenuates lipopolysaccharide‑induced acute lung injury by targeting IL1RN

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