miR-708-5p Regulates Myoblast Proliferation and Differentiation

Xu, Xueli; Liu, Hui; Xu, Dong; Zhang, Yu; Ai, Nini; Wang, Kaiming; Li, Xintong; He, Jun; Jiang, Jun; Ma, Huimin; Zhang, Yuebo

doi:10.3390/vetsci9110641

Cited by 5 publications

(2 citation statements)

References 38 publications

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“…3,4 In these applications, the intricate process of myoblast proliferation is essential for muscle growth and regeneration in bovine species and involves a complex interplay of different regulatory elements and signaling pathways. 5,6 However, the molecular and cellular mechanisms controlling the growth and development of skeletal muscle are still not fully understood. 7−9 Understanding these mechanisms is important not only for optimizing beef production but also for advancing techniques in tissue regeneration and in vitro meat production.…”

Section: ■ Introductionmentioning

confidence: 99%

“…From the perspective of livestock production, muscle growth and regeneration play crucial roles in skeletal muscle development, directly impacting meat production performance and economic value. , Furthermore, the significance of myoblast growth goes beyond traditional animal breeding and encompasses emerging fields such as tissue regeneration and in vitro meat production. , In these applications, the intricate process of myoblast proliferation is essential for muscle growth and regeneration in bovine species and involves a complex interplay of different regulatory elements and signaling pathways. , However, the molecular and cellular mechanisms controlling the growth and development of skeletal muscle are still not fully understood. − Understanding these mechanisms is important not only for optimizing beef production but also for advancing techniques in tissue regeneration and in vitro meat production. , …”

Section: Introductionmentioning

confidence: 99%

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Knockdown of NFIC Promotes Bovine Myoblast Proliferation through the CENPF/CDK1 Axis

Wang,

Guo,

et al. 2024

J. Agric. Food Chem.

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As cellular transcription factors and DNA replicators, nuclear factor I (NFI) family members play an important role in mammalian development. However, there is still a lack of research on the muscle regeneration of NFI family members in cattle. In this study, the analysis of NFI family factors was conducted on their characterization, phylogenetics, and functional domains. We found that NFI family members were relatively conserved among different species, but there was heterogeneity in amino acid sequences, DNA coding sequences, and functional domain among members. Furthermore, among NFI family factors, we observed that NFIC exhibited highly expression in bovine muscle tissues, particularly influencing the expression of proliferation marker genes in myoblasts. To investigate the influence of NFIC on myoblast proliferation, we knocked down NFIC (si-NFIC) and found that the proliferation of myoblasts was significantly promoted. In terms of regulation mechanism, we identified that si-NFIC could counteract the inhibitory effect of the cell cycle inhibitor RO-3306. Interestingly, CENPF, as the downstream target gene of NFIC, could affect the expression of CDK1, CCNB1, and actively regulate the cell cycle pathway and cell proliferation. In addition, when CENPF was knocked down, the phosphorylation of p53 and the expression of Bax were increased, but the expression of Bcl2 was inhibited. Our findings mainly highlight the mechanism by which NFIC acts on the CENPF/CDK1 axis to regulate the proliferation of bovine myoblasts.

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Section: ■ Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Knockdown of NFIC Promotes Bovine Myoblast Proliferation through the CENPF/CDK1 Axis

Wang,

Guo,

et al. 2024

J. Agric. Food Chem.

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Circ‐ECH1 May Compete With miR‐708‐5p to Regulate Ntrk2 in Bronchopulmonary Dysplasia

Cheng,

Li,

Tang

et al. 2024

J of Cellular Biochemistry

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Bronchopulmonary dysplasia (BPD) affects patients' quality of life. Circular RNAs participated in BPD. However, circ‐ECH1's role in BPD has not been reported yet. This study aimed to explore the role and mechanism of circ‐ECH1 in BPD. Hyperoxia‐treated type II alveolar epithelial cells (L2 cells) were used as the in vitro BPD model. CCK‐8, flow cytometry, and reactive oxygen species (ROS) were used to evaluate cell viability. Fluorescence in situ hybridization confirmed the subcellular localization. Circ‐ECH1 overexpression (or inhibited) and miR‐708‐5p mimics were used to investigate the roles of circ‐ECH1 and miR‐708‐5p in BPD. Quantitative reverse‐transcription polymerase reaction (qRT‐PCR) detected the expressions of circ‐ECH1, miR‐708‐5p, and neurotrophic receptor tyrosine kinase 2 (Ntrk2). Ntrk2 expression was evaluated by Western blot analysis. Changes in lung tissues were evaluated by hematoxylin and eosin staining. Pulmonary fibrosis was examined by Mason staining. TUNEL staining was performed to evaluate cell apoptosis in lung tissues. RNA sequencing was performed in the lung tissues of BPD rats. The binding between circ‐ECH1 and miR‐708‐5p was confirmed through dual luciferase activity. Hyperoxia reduced cell viability and increased cell apoptosis and ROS accumulation. In addition, hyperoxia decreased the expression levels of circ‐ECH1, which is mainly located in the cytoplasm. Circ‐ECH1 overexpression increased cell viability but reduced cell apoptosis and ROS accumulation. On the contrary, interference with circ‐ECH1 further promoted cell apoptosis and reduced cell activity. Furthermore, circ‐ECH1 overexpression reduced the incidence of pulmonary fibrosis and lung cell apoptosis. RNA sequencing, followed by qRT‐PCR, confirmed that the expressions of Ntrk2 and miR‐708‐5p were affected by circ‐ECH1. miR‐708‐5p mimics reversed the role of circ‐ECH1 in the BPD. Mechanistically, circ‐ECH1 may bind with miR‐708‐5p to regulate Ntrk2 expression. Circ‐ECH1 may compet with miR‐708‐5p to regulate Ntrk2 expression in BPD. The findings provided a new target for BPD treatment.

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A comprehensive atlas of pig RNA editome across 23 tissues reveals RNA editing affecting interaction mRNA–miRNAs

Long,

Liu,

Fan

et al. 2024

G3: Genes, Genomes, Genetics

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RNA editing is a co-transcriptional/post-transcriptional modification that is mediated by the ADAR enzyme family. Profiling of RNA editing is very limited in pigs. In this study, we collated 3813 RNA-seq data from the public repositories across 23 tissues and carried out comprehensive profiling of RNA editing in pigs. In total, 127,927 A-to-I RNA editing sites were detected. Our analysis showed that 98.2% of RNA editing sites were located within repeat regions, primarily within the pig-specific SINE retrotransposon PRE-1/Pre0_SS elements. Subsequently, we focused on analyzing specific editing sites (SESs) in skeletal muscle tissues. Functional enrichment analyses suggested that they were enriched in signaling pathways associated with muscle cell differentiation, including DMD, MYOD1 and CAV1 genes. Furthermore, we discovered that RNA editing event in the 3`UTR of CFLAR mRNA influenced miR-708-5p binding in this region. In this study, the panoramic RNA editing landscape of different tissues of pigs was systematically mapped, and RNA editing sites and genes involved in muscle cell differentiation were identified. In summary, we identified modifications to pig RNA editing sites and provided candidate targets for further validation.

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miR-708-5p Regulates Myoblast Proliferation and Differentiation

Cited by 5 publications

References 38 publications

Knockdown of NFIC Promotes Bovine Myoblast Proliferation through the CENPF/CDK1 Axis

Knockdown of NFIC Promotes Bovine Myoblast Proliferation through the CENPF/CDK1 Axis

Circ‐ECH1 May Compete With miR‐708‐5p to Regulate Ntrk2 in Bronchopulmonary Dysplasia

A comprehensive atlas of pig RNA editome across 23 tissues reveals RNA editing affecting interaction mRNA–miRNAs

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