Interleukin‐8 enhances myocilin expression, Akt‐FoxO3 signaling and myogenic differentiation in rat skeletal muscle cells

Milewska, Magdalena; Domoradzki, Tomasz; Majewska, Alicja; Błaszczyk, Maciej; Gajewska, Małgorzata; Hulanicka, Magdalena; Ciecierska, Anna; Grzelkowska-Kowalczyk, Katarzyna

doi:10.1002/jcp.28568

Cited by 17 publications

(15 citation statements)

References 68 publications

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“…IL-8-neutralizing antibody impairs the differentiation of hMBs ( Polesskaya et al, 2016 ). In contrast, IL-8 treatment decreases the myogenin/MyoD ratio and embryonic MHC expression in rat myoblasts ( Milewska et al, 2019 ). An appropriate level of IL-8 is important for normal myogenesis.…”

Section: Discussionmentioning

confidence: 99%

Myogenetic Oligodeoxynucleotide (myoDN) Recovers the Differentiation of Skeletal Muscle Myoblasts Deteriorated by Diabetes Mellitus

et al. 2021

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Skeletal muscle wasting in patients with diabetes mellitus (DM) is a complication of decreased muscle mass and strength, and is a serious risk factor that may result in mortality. Deteriorated differentiation of muscle precursor cells, called myoblasts, in DM patients is considered to be one of the causes of muscle wasting. We recently developed myogenetic oligodeoxynucleotides (myoDNs), which are 18-base single-strand DNAs that promote myoblast differentiation by targeting nucleolin. Herein, we report the applicability of a myoDN, iSN04, to myoblasts isolated from patients with type 1 and type 2 DM. Myogenesis of DM myoblasts was exacerbated concordantly with a delayed shift of myogenic transcription and induction of interleukins. Analogous phenotypes were reproduced in healthy myoblasts cultured with excessive glucose or palmitic acid, mimicking hyperglycemia or hyperlipidemia. iSN04 treatment recovered the deteriorated differentiation of plural DM myoblasts by downregulating myostatin and interleukin-8 (IL-8). iSN04 also ameliorated the impaired myogenic differentiation induced by glucose or palmitic acid. These results demonstrate that myoDNs can directly facilitate myoblast differentiation in DM patients, making them novel candidates for nucleic acid drugs to treat muscle wasting in patients with DM.

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Section: Discussionmentioning

confidence: 99%

Myogenetic Oligodeoxynucleotide (myoDN) Recovers the Differentiation of Skeletal Muscle Myoblasts Deteriorated by Diabetes Mellitus

et al. 2021

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“…IL-8-neutralizing antibody impairs the differentiation of hMBs (Polesskaya et al, 2016). In contrast, IL-8 treatment decreases the myogenin/MyoD ratio and embryonic MHC expression in rat myoblasts (Milewska et al, 2019). An appropriate level of IL-8 is important for normal myogenesis.…”

Section: Myodn Recovers Differentiation Of Dm Myoblastsmentioning

confidence: 99%

Myogenetic oligodeoxynucleotide (myoDN) recovers the differentiation of skeletal muscle myoblasts deteriorated by diabetes mellitus

Nakamura

Yonekura

Shimosato

et al. 2021

Preprint

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Sarcopenic obesity is a complication of decreased muscle mass and strength associated with obesity, and sarcopenia associated with diabetes mellitus (DM) is a serious risk factor that may result in mortality. Deteriorated differentiation of muscle precursor cells, called myoblasts, in DM patients is considered to be one of the causes of muscle atrophy. We recently developed myogenetic oligodeoxynucleotides (myoDNs), which are 18-base single-strand DNAs that promote myoblast differentiation by targeting nucleolin. Herein, we report the applicability of a myoDN, iSN04, to myoblasts isolated from patients with type 1 and type 2 DM. Myogenesis of DM myoblasts was exacerbated concordantly with a delayed shift of myogenic transcription and induction of interleukins. Analogous phenotypes were reproduced in healthy myoblasts cultured with excessive glucose or palmitic acid, mimicking hyperglycemia or hyperlipidemia. iSN04 treatment recovered the deteriorated differentiation of plural DM myoblasts by downregulating myostatin and interleukin-8. iSN04 also ameliorated the impaired myogenic differentiation induced by glucose or palmitic acid. These results demonstrate that myoDNs can directly facilitate myoblast differentiation in DM patients, making them novel candidates for nucleic acid drugs to treat sarcopenic obesity.

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“…KEGG pathway enrichment analysis showed that these differentially expressed genes were mainly involved in the PI3K-Akt signaling pathway, regulation of actin cytoskeleton, focal adhesion, and MAPK signaling pathway ( Figure 4F). Among these differentially expressed genes, CCND1 [42], PLCB1 [43], MEF2C [44], and FOXO3 [45,46] have a known function in regulating myogenesis. As a consequence, MEG3 could specifically have important effects on skeletal muscle development.…”

Section: Gene Expression Profile Of Meg3 Knockdown In Porcine Satellimentioning

confidence: 99%

MEG3 Promotes Differentiation of Porcine Satellite Cells by Sponging miR-423-5p to Relieve Inhibiting Effect on SRF

Cheng

Long

Shi

et al. 2020

Cells

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Although thousands of long noncoding RNAs (lncRNAs) have been identified in porcine growth and development, the regulation mechanisms of functional lncRNAs have not been well explored. In this study, using 5′- and 3′-rapid amplification of cDNA ends (RACE) assays, we obtained two different variants of lncRNA maternally expressed gene 3 (MEG3), namely, MEG3 v1 and MEG3 v2, that were both highly expressed in porcine skeletal muscle and in the early stage of the differentiation of porcine satellite cells. Moreover, we identified the core transcript MEG3 v2. Functional analyses showed that MEG3 overexpression could effectively arrest myoblasts in the G1 phase, inhibit DNA replication, and promote myoblast differentiation, whereas MEG3 knockdown resulted in the opposite effects. Interestingly, the expression of serum response factor (SRF), a crucial transcription factor for myogenesis process, remarkably increased and decreased in mRNA and protein levels with the respective overexpression and knockdown of MEG3. Dual luciferase reporter assay showed that MEG3 could attenuate the decrease of luciferase activity of SRF induced by miR-423-5p in a dose-dependent manner. MEG3 overexpression could relieve the inhibitory effect on SRF and myoblast differentiation induced by miR-423-5p. In addition, results of RNA immunoprecipitation analysis suggested that MEG3 could act as a ceRNA for miR-423-5p. Our findings initially established a novel connection among MEG3, miR-423-5p, and SRF in porcine satellite cell differentiation. This novel role of MEG3 may shed new light on understanding of molecular regulation of lncRNA in porcine myogenesis.

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Interleukin‐8 enhances myocilin expression, Akt‐FoxO3 signaling and myogenic differentiation in rat skeletal muscle cells

Cited by 17 publications

References 68 publications

Myogenetic Oligodeoxynucleotide (myoDN) Recovers the Differentiation of Skeletal Muscle Myoblasts Deteriorated by Diabetes Mellitus

Myogenetic Oligodeoxynucleotide (myoDN) Recovers the Differentiation of Skeletal Muscle Myoblasts Deteriorated by Diabetes Mellitus

Myogenetic oligodeoxynucleotide (myoDN) recovers the differentiation of skeletal muscle myoblasts deteriorated by diabetes mellitus

MEG3 Promotes Differentiation of Porcine Satellite Cells by Sponging miR-423-5p to Relieve Inhibiting Effect on SRF

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