IGF-1 receptor mediates differentiation of primary cultures of mouse skeletal myoblasts

Galvin, Conor; Hardiman, Orla; Nolan, Catherine M.

doi:10.1016/s0303-7207(02)00420-3

Cited by 35 publications

(26 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Both growth hormone and insulin can induce SOCS-3 mRNA expression in muscle (29,30), although neither growth hormone or insulin are necessary for myoblast differentiation. However, IGF-I is necessary for differentiation (10), and myoblast production of IGF-I increases during the differentiation process (3); therefore IGF-I could induce SOCS-3 expression. IGF-I mRNA expression increases in C2C12 myoblasts after 48 h of differentiation ( Fig.…”

Section: Statisticsmentioning

confidence: 99%

“…The 2.0-kb SOCS-3 promoter was significantly increased after exposure to 15 and 30 ng/ml of recombinant IGF-I when compared with the myoblasts not treated with exogenous IGF-I, respectively. To determine whether IGF-I was necessary for induction of transcriptional activity of the SOCS-3 promoter, C2C12 myoblasts were induced to differentiate in the presence of a specific IGF-I receptor antibody (␣IR3, 3 g/ml), which prevents the activation of the IGF-I receptor during myoblast differentiation (10). Inclusion of the antibody significantly reduced SOCS-3 promoter activity after 72 h of differentiation; however receptor inhibition did not completely reduce activity to base-line levels (dashed line) (Fig.…”

Section: Statisticsmentioning

confidence: 99%

“…* indicates a value statistically different from the control group (p Ͻ 0.05). C, 2.0-kb SOCS-3 promoter activity was reduced during C2C12 myoblast differentiation when the IGF-I receptor was inhibited with a monoclonal antibody (␣IR3) as previously described (10). C2C12 myoblasts were transiently transfected with the 2.0-kb SOCS-3 promoter.…”

Section: Statisticsmentioning

confidence: 99%

“…Because insulin and IGF-I share many signaling properties, it is possible that SOCS-3 may regulate IGF-I signaling as well. Indeed, Dey et al (9) described an interaction between SOCS-3 and the IGF-I receptor in embryonic kidney 293 cells, and because the activation of the IGF-I receptor is critical for the induction of myoblast differentiation (10), it is possible that SOCS-3 is critical for myoblast differentiation. SOCS-3 is expressed in skeletal muscle (11,12); however a mechanistic role for the expression of SOCS-3 in skeletal muscle has yet to be defined.…”

mentioning

confidence: 99%

See 3 more Smart Citations

SOCS-3 Induces Myoblast Differentiation

Spangenburg

2005

Journal of Biological Chemistry

View full text Add to dashboard Cite

Myoblast differentiation is characterized by a sequence of events that includes an increase in insulinlike growth factor (IGF)-I and contractile gene expression. The increase in IGF-I expression activates cell signaling mechanisms that participate in the differentiation process. One potential contributor is the SOCS-3 (suppressor of cytokine signaling-3) gene, which regulates signaling mechanisms and may be sensitive to changes in IGF-I concentrations. For the first time, the role of SOCS-3 is investigated in myoblast differentiation. SOCS-3 mRNA levels and SOCS-3 transcriptional activity increase during myoblast differentiation. SOCS-3 gene expression is induced, at least in part, by activation of the IGF-I receptor during myoblast differentiation. Overexpression of SOCS-3 cDNA significantly increased transcriptional activation of the 2.0-kb skeletal ␣-actin promoter in differentiating C2C12 myoblasts. In addition, overexpression of SOCS-3 specifically increased serum response factor-driven transcriptional activity but had no effect on nuclear-factor of activated T cell-driven transcriptional activity. SOCS-3 overexpression induced skeletal ␣-actin transcription in a myoblast cell line that cannot respond to endogenous IGF-I, indicating that SOCS-3 can contribute to the myoblast differentiation process in the absence of IGF-I. These data suggest that IGF-I induces myoblast differentiation, in part, by increasing SOCS-3 expression.

show abstract

Section: Statisticsmentioning

confidence: 99%

Section: Statisticsmentioning

confidence: 99%

Section: Statisticsmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

SOCS-3 Induces Myoblast Differentiation

Spangenburg

2005

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…IGF-I은 근육 세포의 증식 및 분화 과정에 있어 중심적인 역할을 할 뿐만 아니라 [10,11], 근육 관련 유전자들의 발현 및 전사 활성화를 증가시키고, 근단백질의 합성을 증가시킨다 [10,11,18,23]. 또한 염증 사이토카인 인 tumor necrosis factor-α (TNF-α)와 interleukin-1, 6 (IL-1,6) 등으로 인해 활성화되는 ubiquitin 합성 효소들의 발현을 억제함으로써 근위축의 진행을 억제하는 기 능을 한다 [12].…”

Section: 서 론unclassified

Effects of Insulin-Like Growth Factor-I on Expression of Suppressor of Cytokine Signaling-3 in C2C12 Myotube

Kim¹,

Won-Jun²

2011

Journal of Life Science

View full text Add to dashboard Cite

Expression of the human β3 integrin subunit in mouse smooth muscle cells enhances IGF‐I‐stimulated signaling and proliferation

Maile

Yoo

et al. 2007

Journal Cellular Physiology

View full text Add to dashboard Cite

Optimal stimulation of signal transduction and biological functions by IGF-I in porcine smooth muscle cells (pSMC) requires ligand occupancy of the alphaVbeta3 integrin. Binding of heparin-binding domain (HBD) of vitronectin (VN) to the cysteine loop (C-loop) region of beta3 is required for pSMC to respond optimally to IGF-I stimulation. Mouse smooth muscle cells (mSMC), which express a form of beta3 whose sequence within the C-loop region is different than porcine or human beta3, do not respond optimally to IGF-I, and IGF-I stimulated beta3 and SHPS-1 phosphorylation which are necessary for optimal IGF-I signaling were undetectable. VN also had no effect on IGF-I stimulated the cell proliferation. In contrast, when human beta3 (hbeta3) was introduced into mSMC, there was an enhanced VN binding in spite of an equivalent amount of total beta3 expression, and IGF-I-dependent beta3, and SHPS-1 phosphorylation were detected. In addition, there was enhanced IGF-I-stimulated Shc association with SHPS-1, Shc tyrosine phosphorylation, Shc and Grb2 association, and MAP kinase activation leading to increased cell proliferation. These enhancements could be further augmented by adding a peptide containing the HBD of VN. To determine if these changes were mediated by the C-loop region of beta3, an antibody that reacts with that region of beta3 was utilized. The addition of the hbeta3 C-loop antibody abolished VN-induced enhancement of IGF-I signaling and IGF-I-stimulated cell proliferation. These results strongly support the conclusion that optimal SMC responsiveness to IGF-I requires ligand interaction with the C-loop domain of hbeta3.

show abstract

IGF-1 receptor mediates differentiation of primary cultures of mouse skeletal myoblasts

Cited by 35 publications

References 61 publications

SOCS-3 Induces Myoblast Differentiation

SOCS-3 Induces Myoblast Differentiation

Effects of Insulin-Like Growth Factor-I on Expression of Suppressor of Cytokine Signaling-3 in C2C12 Myotube

Expression of the human β3 integrin subunit in mouse smooth muscle cells enhances IGF‐I‐stimulated signaling and proliferation

Contact Info

Product

Resources

About