Characterisation of the IGF system in a primary adult human skeletal muscle cell model, and comparison of the effects of insulin and IGF-I on protein metabolism

Crown, Anna; He, X. L.; Holly, Jeff M.P.; Lightman, Stafford L.; Stewart, Claire E.

doi:10.1677/joe.0.1670403

Cited by 48 publications

(39 citation statements)

References 41 publications

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“…The vast majority of in vitro and in vivo studies have indicated that IGF-I stimulates muscle protein synthesis (19,26,38,65). This effect is consistent with the well-established role of IGF in adding new synthetic capacity to muscle fibers by incorporation of new muscle nuclei via stimulation of myoblast or satellite cell proliferation and differentiation (5,12).…”

Section: Discussionsupporting

confidence: 74%

Muscle-specific overexpression of the type 1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3K, and not calcineurin, signaling

Quinn¹,

Anderson²,

Plymate³

2007

American Journal of Physiology-Endocrinology and Metabolism

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Quinn LS, Anderson BG, Plymate SR. Muscle-specific overexpression of the type 1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3K, and not calcineurin, signaling. Am J Physiol Endocrinol Metab 293: E1538-E1551, 2007. First published October 16, 2007; doi:10.1152/ajpendo.00160.2007.-The insulinlike growth factors (IGF-I and IGF-II), working through the type 1 IGF receptor (IGF-1R), are key mediators of skeletal muscle fiber growth and hypertrophy. These processes are largely dependent on stimulation of proliferation and differentiation of muscle precursor cells, termed myoblasts. It has not been rigorously determined whether the IGFs can also mediate skeletal muscle hypertrophy in a myoblast-independent fashion. Similarly, although the phosphatidylinositol 3-kinase (PI3K) and calcineurin signaling pathways have been implicated in skeletal muscle hypertrophy, these pathways are also involved in skeletal myoblast differentiation. To determine whether the IGFs can stimulate skeletal muscle hypertrophy in a myoblast-independent fashion, we developed and validated a retroviral expression vector that mediated overexpression of the human IGF-1R in rat L6 skeletal myotubes (immature muscle fibers), but not in myoblasts. L6 myotubes transduced with this vector accumulated significantly higher amounts of myofibrillar proteins, in a ligand-and receptor-dependent manner, than controls and demonstrated significantly increased rates of protein synthesis. Stimulation of myotube hypertrophy was independent of myoblast contributions, inasmuch as these cultures did not exhibit increased levels of myoblast proliferation or differentiation. Experiments with PI3K and calcineurin inhibitors indicated that myoblast-independent myotube hypertrophy was mediated by PI3K, but not calcineurin, signaling. This study demonstrates that IGF can mediate skeletal muscle hypertrophy in a myoblast-independent fashion and suggests that muscle-specific overexpression of the IGF-1R or stimulation of its signaling pathways could be used to develop strategies to ameliorate muscle wasting without stimulating proliferative pathways leading to carcinogenesis or other pathological sequelae.insulin-like growth factor; insulin-like growth factor receptor; protein synthesis; protein degradation; sarcopenia THE INSULIN-LIKE GROWTH FACTORS (IGF-I and IGF-II), signaling via the type 1 IGF receptor (IGF-1R) are crucial mediators of skeletal muscle development, hypertrophy, and regeneration (7,29,33,46,60). IGF signaling is required for fetal skeletal muscle development (7,29,46,60), a process largely dependent on the proliferation and differentiation of muscle precursor cells known as myoblasts (5,12,29,51,60). Cell culture studies have shown that the IGFs are strong stimulators of myoblast proliferation and differentiation (15,20,29). Overexpression of the IGF-1R via constitutive promoters in skeletal myogenic cell lines and primary skeletal myogenic cultures also resulted in greatly enhanced proliferation and differentiation responses to I...

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Section: Discussionsupporting

confidence: 74%

Muscle-specific overexpression of the type 1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3K, and not calcineurin, signaling

Quinn¹,

Anderson²,

Plymate³

2007

American Journal of Physiology-Endocrinology and Metabolism

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“…In contrast, IGF-II gene expression was decreased in turkey satellite cells from proliferation to differentiation (Ernst et al, 1996). In addition, IGF-I expression was not detected in humans (Crown et al, 2000) or avian (Kocamis et al, 2001) satellite cells. The expression patterns of IGF for in vitro muscle cells suggested autocrine regulation of myogenesis by IGFs (Wang et al, 2011).…”

Section: Discussionmentioning

confidence: 79%

Association between DLK1 and IGF-I gene expression and meat quality in sheep

Su¹,

Sun²,

Li³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The aim of the present study was to detect delta-like 1 homolog (DLK1) and insulin-like growth factor-I (IGF-I) gene expression in the longissimus dorsi of Hu sheep at different growth stages and study the association between these genes and meat quality. The diameter and density of muscle fibers and tenderness of the longissimus dorsi were measured. Growth stage, but not sex, significantly affected DLK1 and IGF-I expression. DLK1 and IGF-I expression in the sheep longissimus dorsi gradually increased with growth, but also decreased during some periods. These results suggest that different growth stages significantly affect DLK1 and IGF-I gene expression in sheep muscle tissue. The expression of DLK1 and IGF-I genes were positively and significantly (P < 0.01) correlated with muscle fiber diameter and muscle fiber shear stress, and negatively and significantly (P < 0.01) correlated with muscle fiber density. Muscle fiber diameter was positively and significantly (P < 0.01) correlated with muscle fiber shear stress, and negatively and significantly (P < 0.01) correlated with muscle fiber density. In addition,

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“…Many studies have confirmed that the IGF-1 and insulin signaling pathways play important roles in the proliferation of myoblasts and the progression of myogenesis. IGF-1 and insulin have been shown to stimulate the proliferation and differentiation of muscle cells in a time-and concentrationdependent manner (Allen et al, 1985;Cassar-Malek et al, 1999;Cen et al, 2008;Engert et al, 1996;Grabiec et al, 2014); these important mediators also modulate protein metabolism (Castillo et al, 2004;Crown et al, 2000;Fryburg, 1994). Moreover, the myogenesis program can be influenced when the expression of IGF-1 and insulin receptors are altered (Arabkhari et al, 2010;Bonnesen et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

The NF-κB-modulated microRNAs miR-195 and miR-497 inhibit myoblast proliferation by targeting Igf1r, Insr and cyclin genes

Wei

Zhang

Bai

et al. 2016

Journal of Cell Science

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MicroRNAs (miRNAs) play important roles in the development of skeletal muscle. In our previous study, expression of miR-195 and miR-497 were shown to be upregulated during muscle development in pigs. In this study, we investigated the roles of these two miRNAs in myogenesis and analyzed their transcriptional regulation. Our results showed that miR-195 and miR-497 were upregulated during muscle development and myoblast differentiation. Moreover, miR-195 and miR-497 inhibited proliferation but not differentiation in C2C12 cells. Further investigation revealed that Igf1r, Insr, Ccnd2 and Ccne1 were directly targeted by miR-195 and miR-497 in myoblasts. In addition, we confirmed that miR-195 and miR-497, which shared the similar expression profiling, were negatively regulated by nuclear factor κB (NF-κB) in both myoblasts and skeletal muscle tissue. Our data illustrate that the signaling pathway NF-κB-miR-195/497-Igf1r/InsrCcnd2/Ccne1 plays important roles in myogenesis. Our study provides novel evidence for the roles of miR-195 and miR-497 in muscle development.

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Characterisation of the IGF system in a primary adult human skeletal muscle cell model, and comparison of the effects of insulin and IGF-I on protein metabolism

Cited by 48 publications

References 41 publications

Muscle-specific overexpression of the type 1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3K, and not calcineurin, signaling

Muscle-specific overexpression of the type 1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3K, and not calcineurin, signaling

Association between DLK1 and IGF-I gene expression and meat quality in sheep

The NF-κB-modulated microRNAs miR-195 and miR-497 inhibit myoblast proliferation by targeting Igf1r, Insr and cyclin genes

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