The miRNA‐143‐3p–Sox6–Myh7 pathway is altered in obesogenic diet‐induced cardiac hypertrophy

Silva, Tábatha de Oliveira; Lino, Caroline Antunes; Miranda, Jarbas Honório de; Balbino-Silva, Camila S.; Lunardon, Guilherme; Lima, Vanessa Batista de Sousa; Jensen, Leonardo; Donato, José; Irigoyen, Maria Cláudia; Barreto‐Chaves, Maria Luíza Morais; Diniz, Gabriela Placoná

doi:10.1113/ep090315

Cited by 7 publications

(3 citation statements)

References 62 publications

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“…These results suggest that miR-24-3p may regulate skeletal muscle fiber type transformation by binding to these gene clusters ( Mapk14 , Nek4 , Pskh1 , Pim1 , and Nlk ). Furthermore, it has been shown that many genes are involved in skeletal muscle regeneration and myofiber type transformation, such as MEETL8 and SOX6 inhibiting slow myogenesis by suppressing MYH7 expression [ 66 , 67 ], and Map3k20 and LSD1 playing important roles in regulating skeletal muscle regeneration [ 68 , 69 ]. We speculate that miR-24-3p may also target these genes in regulating myofiber type transformation and skeletal muscle regeneration.…”

Section: Discussionmentioning

confidence: 99%

Regulation of myo-miR-24-3p on the Myogenesis and Fiber Type Transformation of Skeletal Muscle

Fan,

Yao,

Liu

et al. 2024

Genes

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Skeletal muscle plays critical roles in providing a protein source and contributing to meat production. It is well known that microRNAs (miRNAs) exert important effects on various biological processes in muscle, including cell fate determination, muscle fiber morphology, and structure development. However, the role of miRNA in skeletal muscle development remains incompletely understood. In this study, we observed a critical miRNA, miR-24-3p, which exhibited higher expression levels in Tongcheng (obese-type) pigs compared to Landrace (lean-type) pigs. Furthermore, we found that miR-24-3p was highly expressed in the dorsal muscle of pigs and the quadriceps muscle of mice. Functionally, miR-24-3p was found to inhibit proliferation and promote differentiation in muscle cells. Additionally, miR-24-3p was shown to facilitate the conversion of slow muscle fibers to fast muscle fibers and influence the expression of GLUT4, a glucose transporter. Moreover, in a mouse model of skeletal muscle injury, we demonstrated that overexpression of miR-24-3p promoted rapid myogenesis and contributed to skeletal muscle regeneration. Furthermore, miR-24-3p was found to regulate the expression of target genes, including Nek4, Pim1, Nlk, Pskh1, and Mapk14. Collectively, our findings provide evidence that miR-24-3p plays a regulatory role in myogenesis and fiber type conversion. These findings contribute to our understanding of human muscle health and have implications for improving meat production traits in livestock.

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Section: Discussionmentioning

confidence: 99%

Regulation of myo-miR-24-3p on the Myogenesis and Fiber Type Transformation of Skeletal Muscle

Fan,

Yao,

Liu

et al. 2024

Genes

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“…MiRNA deregulation is frequent during CH [25]. As an example, miR-143-3p is related to the development of CH induced by an obesogenic diet [26]. Moreover, targeting miR-30b has been proposed as a potential therapy in CH [27].…”

Section: Discussionmentioning

confidence: 99%

CircRNA Larp4b/miR-298-5p/Mef2c Regulates Cardiac Hypertrophy Induced by Angiotensin II

Xie,

Xu,

Xiong

et al. 2023

Int J Sports Med

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Cardiac hypertrophy (CH) is an early marker in the clinical course of heart failure. Circular RNAs (circRNAs) play important roles in human disease. However, the role of circ_Larp4b in myocardial hypertrophy has not been studied. Angiotensin II (Ang II) treated HL-1 cells to induce a CH cell model. Quantitative real-time polymerase chain reaction was used to detect the expression of circ_Larp4b, microRNA-298-5p, and myocyte enhancer factor 2 (Mef2c). Western blot detected the protein level of alpha-actinin-2 (ACTN2), beta-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), and Mef2c. The relationship between miR-298-5p and circ_Larp4b or Mef2c was verified by dual-luciferase reporter assay and RNA pull-down assay. Circ_Larp4b and Mef2c were upregulated in HL-1 cells treated with Ang II. Moreover, circ_Larp4b down-regulation regulated the progress of CH induced by Ang II. MiR-298-5p was a target of circ_Larp4b, and Mef2c was a target of miR-298-5p. Overexpressed Mef2c reversed the cell size inhibited by miR-298-5p in Ang II-induced HL-1 cells. Circ_Larp4b regulated CH progress by regulating miR-298-5p/Mef2c axis.

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“…The increase in MYH7 and MYH7B expression and/or transcriptional activity is one of the cascade effects associated with SOX6 inhibition that has been described either in vitro or in animal models. [ 18 , 19 ]. It has been postulated that increased MYH6 leads to upregulation of miR-208a , which in turn inhibits the expression of SOX6 but promotes the activation/upregulation of MYH7B , with subsequent upregulation of miR-499, which is another modulator of SOX6 [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Myosins and MyomiR Network in Patients with Obstructive Hypertrophic Cardiomyopathy

et al. 2022

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Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiomyopathy. The molecular mechanisms determining HCM phenotypes are incompletely understood. Myocardial biopsies were obtained from a group of patients with obstructive HCM (n = 23) selected for surgical myectomy and from 9 unused donor hearts (controls). A subset of tissue-abundant myectomy samples from HCM (n = 10) and controls (n = 6) was submitted to laser-capture microdissection to isolate cardiomyocytes. We investigated the relationship among clinical phenotype, cardiac myosin proteins (MyHC6, MyHC7, and MyHC7b) measured by optimized label-free mass spectrometry, the relative genes (MYH7, MYH7B and MYLC2), and the MyomiR network (myosin-encoded microRNA (miRs) and long-noncoding RNAs (Mhrt)) measured using RNA sequencing and RT-qPCR. MyHC6 was lower in HCM vs. controls, whilst MyHC7, MyHC7b, and MyLC2 were comparable. MYH7, MYH7B, and MYLC2 were higher in HCM whilst MYH6, miR-208a, miR-208b, miR-499 were comparable in HCM and controls. These results are compatible with defective transcription by active genes in HCM. Mhrt and two miR-499-target genes, SOX6 and PTBP3, were upregulated in HCM. The presence of HCM-associated mutations correlated with PTBP3 in myectomies and with SOX6 in cardiomyocytes. Additionally, iPSC-derived cardiomyocytes, transiently transfected with either miR-208a or miR-499, demonstrated a time-dependent relationship between MyomiRs and myosin genes. The transfection end-stage pattern was at least in part similar to findings in HCM myectomies. These data support uncoupling between myosin protein/genes and a modulatory role for the myosin/MyomiR network in the HCM myocardium, possibly contributing to phenotypic diversity and providing putative therapeutic targets.

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The miRNA‐143‐3p–Sox6–Myh7 pathway is altered in obesogenic diet‐induced cardiac hypertrophy

Cited by 7 publications

References 62 publications

Regulation of myo-miR-24-3p on the Myogenesis and Fiber Type Transformation of Skeletal Muscle

Regulation of myo-miR-24-3p on the Myogenesis and Fiber Type Transformation of Skeletal Muscle

CircRNA Larp4b/miR-298-5p/Mef2c Regulates Cardiac Hypertrophy Induced by Angiotensin II

Myosins and MyomiR Network in Patients with Obstructive Hypertrophic Cardiomyopathy

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