MiR-183-5p induced by saturated fatty acids regulates the myogenic differentiation by directly targeting FHL1 in C2C12 myoblasts

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

doi:10.5483/bmbrep.2020.53.11.175

Cited by 12 publications

(11 citation statements)

References 31 publications

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“…The miR-183 family gene cluster plays multiple roles in a wide range of physiological and pathological processes, such as cell proliferation, apoptosis, and metabolism [ 35 ]. The overexpression of miR-183-5p inhibits the myogenic differentiation of C2C12 myoblasts [ 36 ]. MiR-106b has been found to regulate cellular cholesterol efflux by targeting ABCA1 in macrophages [ 37 ], miR-106 plays a role in various dystrophies such as facioscapulohumeral muscular dystrophy, limb-girdle muscular dystrophies, and Miyoshi myopathy [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Integrative analysis of circRNA, miRNA, and mRNA profiles to reveal ceRNA regulation in chicken muscle development from the embryonic to post-hatching periods

Lei

Han

et al. 2022

BMC Genomics

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Background The growth and development of skeletal muscle are regulated by protein-coding genes and non-coding RNA. Circular RNA (circRNA) is a type of non-coding RNA involved in a variety of biological processes, especially in post-transcriptional regulation. To better understand the regulatory mechanism of circRNAs during the development of muscle in chicken, we performed RNA-seq with linear RNA depletion for chicken breast muscle in 12 (E 12) and17 (E 17) day embryos, and 1 (D 1), 14 (D 14), 56 (D 56), and 98 (D 98) days post-hatch. Results We identified 5755 differentially expressed (DE)-circRNAs during muscle development. We profiled the expression of DE-circRNAs and mRNAs (identified in our previous study) at up to six time points during chicken muscle development and uncovered a significant profile (profile 16) for circRNA upregulation during aging in muscle tissues. To investigate competing endogenous RNA (ceRNA) regulation in muscle and identify muscle-related circRNAs, we constructed a circRNA-miRNA-mRNA regulatory network using the circRNAs and mRNAs from profile 16 and miRNAs identified in our previous study, which included 361 miRNAs, 68 circRNAs, 599 mRNAs, and 31,063 interacting pairs. Functional annotation showed that upregulated circRNAs might contribute to glycolysis/gluconeogenesis, biosynthesis of amino acids, pyruvate metabolism, carbon metabolism, glycogen and sucrose metabolism through the ceRNA network, and thus affected postnatal muscle development by regulating muscle protein deposition. Of them, circRNA225 and circRNA226 from the same host gene might be key circRNAs that could regulate muscle development by interacting with seven common miRNAs and 207 mRNAs. Our experiments also demonstrated that there were interactions among circRNA225, gga-miR-1306-5p, and heat shock protein alpha 8 (HSPA8). Conclusions Our results suggest that adequate supply of nutrients such as energy and protein after hatching may be a key factor in ensuring chicken yield, and provide several candidate circRNAs for future studies concerning ceRNA regulation during chicken muscle development.

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Section: Discussionmentioning

confidence: 99%

Integrative analysis of circRNA, miRNA, and mRNA profiles to reveal ceRNA regulation in chicken muscle development from the embryonic to post-hatching periods

Lei

Han

et al. 2022

BMC Genomics

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“…Protein concentrations were measured using the Bradford assay (Bio-Rad, USA). Western blot analysis was performed using standard protocols ( 41 ). The following primary antibodies were used: PPARγ (2435s, CST), C/EBPα (2295, CST), C/EBPβ (sc7962, Santa Cruz), FABP4 (2120s, CST), Akt (9272s, CST), p-Akt (9271s, CST), AMPKα (2532s, CST), p-AMPKα (2535s, CST), β-Catenin (06-734, Sigma), p38 (9212s, CST), p-p38 (9215s, CST), ERK (9102s, CST), p-ERK (9106s, CST), JNK (9252s, CST), p-JNK (9251s, CST), CHOP (2895s, CST), and HSP90 (sc-13119, Santa Cruz).…”

Section: Methodsmentioning

confidence: 99%

Myonectin inhibits adipogenesis in 3T3-L1 preadipocytes by regulating p38 MAPK pathway

Park

Kim

et al. 2021

BMB Rep.

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In current times, obesity is a major health problem closely associated with metabolic disease such as diabetes, dyslipidemia, and cardiovascular disease. The direct cause of obesity is known as an abnormal increase in fat cell size and the adipocyte pool. Hyperplasia, the increase in number of adipocytes, results from adipogenesis in which preadipocytes differentiate into mature adipocytes. Adipogenesis is regulated by local and systemic cues that alter transduction pathways and subsequent control of adipogenic transcription factors. Therefore, the regulation of adipogenesis is an important target for preventing obesity. Myonectin, a member of the CTRP family, is a type of myokine released by skeletal muscle cells. Although several studies have shown that myonectin is associated with lipid metabolism, the role of myonectin during adipogenesis is not known. Here, we demonstrate the role of myonectin during adipocyte differentiation of 3T3-L1 cells. We found that myonectin inhibits the adipogenesis of 3T3-L1 preadipocytes with a reduction in the expression of adipogenic transcription factors such as C/EBPα, β and PPARγ. Furthermore, we show that myonectin has an inhibitory effect on adipogenesis through the regulation of the p38 MAPK pathway and CHOP. These findings suggest that myonectin may be a novel therapeutic target for the prevention of obesity.

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“…After differentiation, C2C12 myoblasts were fixed, permeabilized, and visualized with MyHC antibodies, Alexa 488-conjugated goat anti-mouse antibody (Invitrogen), and Hoechst 33342 (Invitrogen), as described previously ( 17 , 31 ). Differentiation indices were calculated by expressing numbers of nuclei in MyHC-positive myotubes as percentages of total numbers of nuclei in fields, and fusion indices were calculated by expressing numbers of myotubes with three or more nuclei as percentages of total numbers of nuclei.…”

Section: Methodsmentioning

confidence: 99%

MiR-141-3p regulates myogenic differentiation in C2C12 myoblasts via CFL2-YAP-mediated mechanotransduction

Nguyen

Lee

2022

BMB Rep

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Skeletal myogenesis is essential to keep muscle mass and integrity, and impaired myogenesis is closely related to the etiology of muscle wasting. Recently, miR-141-3p has been shown to be induced under various conditions associated with muscle wasting, such as aging, oxidative stress, and mitochondrial dysfunction. However, the functional significance and mechanism of miR-141-3p in myogenic differentiation have not been explored to date. In this study, we investigated the roles of miR-141-3p on CFL2 expression, proliferation, and myogenic differentiation in C2C12 myoblasts. MiR-141-3p appeared to target the 3'UTR of CFL2 directly and suppressed the expression of CFL2, an essential factor for actin filament (F-actin) dynamics. Transfection of miR-141-3p mimic in myoblasts increased F-actin formation and augmented nuclear Yes-associated protein (YAP), a key component of mechanotransduction. Furthermore, miR-141-3p mimic increased myoblast proliferation and promoted cell cycle progression throughout the S and G2/M phases. Consequently, miR-141-3p mimic led to significant suppressions of myogenic factors expression, such as MyoD, MyoG, and MyHC, and hindered the myogenic differentiation of myoblasts. Thus, this study reveals the crucial role of miR-141-3p in myogenic differentiation via CFL2-YAP-mediated mechanotransduction and provides implications of miRNA-mediated myogenic regulation in skeletal muscle homeostasis. [BMB Reports 2022; 55(2): 104-109]

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MiR-183-5p induced by saturated fatty acids regulates the myogenic differentiation by directly targeting FHL1 in C2C12 myoblasts

Cited by 12 publications

References 31 publications

Integrative analysis of circRNA, miRNA, and mRNA profiles to reveal ceRNA regulation in chicken muscle development from the embryonic to post-hatching periods

Integrative analysis of circRNA, miRNA, and mRNA profiles to reveal ceRNA regulation in chicken muscle development from the embryonic to post-hatching periods

Myonectin inhibits adipogenesis in 3T3-L1 preadipocytes by regulating p38 MAPK pathway

MiR-141-3p regulates myogenic differentiation in C2C12 myoblasts via CFL2-YAP-mediated mechanotransduction

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