Constitutive and cytokine-induced production of interleukin-6 by human myoblasts

Bartoccioni, Emanuela; Michaelis, Dorothea; Hohlfeld, Reinhard

doi:10.1016/0165-2478(94)90076-0

Cited by 94 publications

(45 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Alternatively, human myoblasts can be induced to produce IL-6, IL-1α, IL-1β and TNF-α in vitro [37-39]. Consistently, we also found, in IFN-γ constructed inflammatory milieu, myoblasts and myotubes up-regulated mRNA levels of IL-1β, IL-6 and MIP-1α, and additionally, myotubes up-regulated TNF-α and MCP-1 levels.…”

Section: Discussionsupporting

confidence: 73%

Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells

Ding

Shi

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Whether calcium/calmodulin-dependent protein kinase IV (CaMKIV) plays a role in regulating immunologic features of muscle cells in inflammatory environment, as it does for immune cells, remains mostly unknown. In this study, we investigated the influence of endogenous CaMKIV on the immunological characteristics of myoblasts and myotubes received IFN-γ stimulation. Methods: C₂C₁₂ and murine myogenic precursor cells (MPCs) were cultured and differentiated in vitro, in the presence of pro-inflammatory IFN-γ. CaMKIV shRNA lentivirus transfection was performed to knockdown CaMKIV gene in C₂C₁₂ cells. pEGFP-N1-CaMKIV plasmid was delivered into knockout cells for recovering intracellular CaMKIV gene level. CREB1 antagonist KG-501 was used to block CREB signal. qPCR, immunoblot analysis, or immunofluorescence was used to detect mRNA and protein levels of CaMKIV, immuno-molecules, or pro-inflammatory cytokines and chemokines. Co-stimulatory molecules expression was assessed by FACS analysis. Results: IFN-γ induces the expression or up-regulation of MHC-I/II and TLR3, and the up-regulation of CaMKIV level in muscle cells. In contrast, CaMKIV knockdown in myoblasts and myotubes leads to expression inhibition of the above immuno-molecules. As well, CaMKIV knockdown selectively inhibits pro-inflammatory cytokines/chemokines, and co-stimulatory molecules expression in IFN-γ treated myoblasts and myotubes. Finally, CaMKIV knockdown abolishes IFN-γ induced CREB pathway molecules accumulation in differentiated myotubes. Conclusions: CaMKIV can be induced to up-regulate in muscle cells under inflammatory condition, and positively mediates intrinsic immune behaviors of muscle cells triggered by IFN-γ.

show abstract

Section: Discussionsupporting

confidence: 73%

Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells

Ding

Shi

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Thus, excessive release of pro-inflammatory molecules originating from adipose tissue might play an important role in the pathogenesis of obesity-related insulin resistance by both autocrine/paracrine and endocrine effects (Festa et al, 2000;Berg and Scherer, 2005;de and Olefsky, 2008). Interestingly, pro-inflammatory cytokines especially IL-6 are also secreted by other insulin target tissues including skeletal muscle (Bartoccioni et al, 1994;Hiscock et al, 2004). However, data from human muscle exercise studies have indicated that IL-6 produced by skeletal muscles might improve insulin sensitivity rather than induce insulin resistance (Helge et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

The anti-diabetic AMPK activator AICAR reduces IL-6 and IL-8 in human adipose tissue and skeletal muscle cells

Lihn

Pedersen

Lund

et al. 2008

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

“…Hence, the n value presented in Table 1 may be lower than the n value presented in the original study. ͓Modified from Fischer (100).͔ Whereas myoblasts had been shown to be capable of producing IL-6 (19,72), endothelial cells (402), fibroblasts (72), and smooth muscle cells (171) had been shown to produce IL-6 under certain circumstances. Langberg et al (185) demonstrated that IL-6 is produced by the peritendinous tissue of active muscle during exercise.…”

Section: B Sources Of Contraction-induced Il-6mentioning

confidence: 99%

Muscle as an Endocrine Organ: Focus on Muscle-Derived Interleukin-6

Pedersen¹,

Febbraio²

2008

Physiological Reviews

1,789

1,646

View full text Add to dashboard Cite

Skeletal muscle has recently been identified as an endocrine organ. It has, therefore, been suggested that cytokines and other peptides that are produced, expressed, and released by muscle fibers and exert paracrine, autocrine, or endocrine effects should be classified as “myokines.” Recent research demonstrates that skeletal muscles can produce and express cytokines belonging to distinctly different families. However, the first identified and most studied myokine is the gp130 receptor cytokine interleukin-6 (IL-6). IL-6 was discovered as a myokine because of the observation that it increases up to 100-fold in the circulation during physical exercise. Identification of IL-6 production by skeletal muscle during physical activity generated renewed interest in the metabolic role of IL-6 because it created a paradox. On one hand, IL-6 is markedly produced and released in the postexercise period when insulin action is enhanced but, on the other hand, IL-6 has been associated with obesity and reduced insulin action. This review focuses on the myokine IL-6, its regulation by exercise, its signaling pathways in skeletal muscle, and its role in metabolism in both health and disease.

show abstract

Constitutive and cytokine-induced production of interleukin-6 by human myoblasts

Cited by 94 publications

References 21 publications

Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells

Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells

The anti-diabetic AMPK activator AICAR reduces IL-6 and IL-8 in human adipose tissue and skeletal muscle cells

Muscle as an Endocrine Organ: Focus on Muscle-Derived Interleukin-6

Contact Info

Product

Resources

About