Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2

Nguyen, Mai Thi Thanh; Min, Kyung-Ho; Lee, Wan

doi:10.3390/ijms222010972

Cited by 9 publications

(8 citation statements)

References 52 publications

(84 reference statements)

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“…Several studies have examined the direct effects of PA on cultured myoblasts and myocytes. Similar to the findings of the present study, treatment of myoblasts with PA has been shown to inhibit myogenic cell differentiation and myotube maturation [ 21 , 22 , 39 , 40 ] and reduce type II myosin protein expression [ 41 ]. We further clarified the detailed mechanism by which PA treatment selectively inhibits the expression of specific MHC isoforms at a transcription level during myoblast differentiation.…”

Section: Discussionsupporting

confidence: 88%

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Palmitic Acid Inhibits Myogenic Activity and Expression of Myosin Heavy Chain MHC IIb in Muscle Cells through Phosphorylation-Dependent MyoD Inactivation

Matsuba

Fujita

Iida

2023

IJMS

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Sarcopenia associated with aging and obesity is characterized by the atrophy of fast-twitch muscle fibers and an increase in intramuscular fat deposits. However, the mechanism of fast-twitch fiber-specific atrophy remains unclear. In this study, we aimed to assess the effect of palmitic acid (PA), the most common fatty acid component of human fat, on muscle fiber type, focusing on the expression of fiber-type-specific myosin heavy chain (MHC). Myotubes differentiated from C2C12 myoblasts were treated with PA. The PA treatment inhibited myotube formation and hypertrophy while reducing the gene expression of MHC IIb and IIx, specific isoforms of fast-twitch fibers. Consistent with this, a significant suppression of MHC IIb protein expression in PA-treated cells was observed. A reporter assay using plasmids containing the MHC IIb gene promoter revealed that the PA-induced reduction in MHC IIb gene expression was caused by the suppression of MyoD transcriptional activity through its phosphorylation. Treatment with a specific protein kinase C (PKC) inhibitor recovered the reduction in MHC IIb gene expression levels in PA-treated cells, suggesting the involvement of the PA-induced activation of PKC. Thus, PA selectively suppresses the mRNA and protein expression of fast-twitch MHC by modulating MyoD activity. This finding provides a potential pathogenic mechanism for age-related sarcopenia.

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Section: Discussionsupporting

confidence: 88%

“…Furthermore, PA has been shown to induce endoplasmic reticulum (ER) stress, which in turn triggers programmed cell death via apoptosis [ 19 , 20 ]. PA also regulates the expression of several microRNAs, thereby inhibiting myoblast differentiation and maturation into myofibers [ 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Palmitic Acid Inhibits Myogenic Activity and Expression of Myosin Heavy Chain MHC IIb in Muscle Cells through Phosphorylation-Dependent MyoD Inactivation

Matsuba

Fujita

Iida

2023

IJMS

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“…Defects in myoblast functions can result in a loss of muscle mass and decline in performance, which are characteristics of patients with sarcopenia. The immortalized murine cell line C2C12 or transformed rat cell line L6 is commonly utilized to study the regulation of metabolism and myogenesis in skeletal muscle cells [ 9 , 10 , 11 , 12 , 25 , 26 , 27 ]. Few studies have utilized in vitro differentiated human myotubes obtained by long-term maintenance of human myoblasts from multiple donors in the presence of recombinant growth hormones [ 13 , 14 , 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Free Fatty Acid Species Differentially Modulate the Inflammatory Gene Response in Primary Human Skeletal Myoblasts

Rauen

Hao

Müller

et al. 2021

Biology

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Age-related loss of skeletal muscle is associated with obesity and inflammation. In animal models, intramuscular fat deposits compromise muscle integrity; however, the relevant fat components that mediate muscular inflammation are not known. Previously, we hypothesized that free fatty acids (FFAs) may directly induce inflammatory gene expression in skeletal muscle cells of obese rats. Here, we examined this hypothesis in primary human skeletal myoblasts (SkMs) using multiplex expression analysis of 39 inflammatory proteins in response to different FFA species. Multiplex mRNA quantification confirmed that the IL6, IL1RA, IL4, LIF, CXCL8, CXCL1, CXCL12 and CCL2 genes were differentially regulated by saturated and unsaturated C16 or C18 FFAs. Fluorescence staining revealed that only saturated C16 and C18 strongly interfere with myoblast replication independent of desmin expression, mitochondrial abundance and oxidative activity. Furthermore, we addressed the possible implications of 71 human receptor tyrosine kinases (RTKs) in FFA-mediated effects. Phosphorylated EphB6 and TNK2 were associated with impaired myoblast replication by saturated C16 and C18 FFAs. Our data suggest that abundant FFA species in human skeletal muscle tissue may play a decisive role in the progression of sarcopenic obesity by affecting inflammatory signals or myoblast replication.

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“…As a result of miRNA sequencing, it was observed that miR-429-3p was highly expressed in a high fat chickens. Furthermore, Nguyen et al [74] examined the role of miR-429-3p on myoblast proliferation and myogenic differentiation in their experiment.…”

Section: Discussionmentioning

confidence: 99%

The evolutionary relationships of microRNAs in the regulation of glucose and lipid metabolism in human and animals

Kılıç

Marakli

2023

IJPTE

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microRNA (miRNA) is a non-coding RNA type, regulating gene expressions at a post-transcriptional level. Changes in miRNA expressions can cause problems such as lipid metabolism disorder, cardiovascular disease, growth retardation, low birth weight and insulin resistance, etc., in human and animals. In this study, we investigated the evolutionary relationships of 14 miRNAs including hsa-miR27a-5p, hsa-miR149-3p, hsa-miR374c-5p, mmu-miR-678, mmu-miR-698-5p, hsa-miR-199a-3p, hsa-miR122-3p, hsa-miR342-3p, mmu-miR201-5p, hsa-miR429, hsa-miR370-3p, hsa-miR130a-5p, hsa-miR330-3p and hsa-miR770-5p related to different metabolic pathways including cardiovascular diseases and lipid metabolism. For this purpose, miRNAs were retrieved from miRBase database. After, Clustal Omega analyses were performed for alignment, and a phylogenetic tree was constructed via MEGA 11. Phylogenetic tree indicated that 14 miRNA sequences were clustered into four groups. One group consisted of mmu-miR-678, and the other 13 sequences were separated into three groups, revealing a close relationship among miRNAs. Findings from different studies provide a new perspective for potential miRNA-based biomarkers to detect lipid metabolism disorders, cardiovascular diseases as well as related disorders.

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Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2

Cited by 9 publications

References 52 publications

Palmitic Acid Inhibits Myogenic Activity and Expression of Myosin Heavy Chain MHC IIb in Muscle Cells through Phosphorylation-Dependent MyoD Inactivation

Palmitic Acid Inhibits Myogenic Activity and Expression of Myosin Heavy Chain MHC IIb in Muscle Cells through Phosphorylation-Dependent MyoD Inactivation

Free Fatty Acid Species Differentially Modulate the Inflammatory Gene Response in Primary Human Skeletal Myoblasts

The evolutionary relationships of microRNAs in the regulation of glucose and lipid metabolism in human and animals

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