Prototypical anti-inflammatory cytokine IL-10 prevents loss of IGF-I-induced myogenin protein expression caused by IL-1β

Strle, Klemen; McCusker, Robert H.; Johnson, Rodney W.; Zunich, Samantha M.; Dantzer, Robert; Kelley, Keith W.

doi:10.1152/ajpendo.00662.2007

Cited by 25 publications

(20 citation statements)

References 56 publications

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“…The relatively higher amounts of IL-10 in CM-LPS compared with CM-P might counteract the relatively lower amounts of TNF␣ and IL-6 and other proinflammatory cytokines present in CM-LPS compared with CM-P. Future studies should define their combined contribution and whether phospho-JNK is responsible for the insulin resistance elicited by CM-P. Regarding the latter, exposure of C 2 C 12 muscle cells to IL-10 diminished the stimulation of JNK phosphorylation by TNF␣ or IL-1␤ (40,41).…”

Section: Discussionmentioning

confidence: 98%

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Samokhvalov¹,

Bilan²,

Schertzer³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Section: Discussionmentioning

confidence: 98%

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Samokhvalov¹,

Bilan²,

Schertzer³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…The increased mRNA expression of IL-1ra and IL-10 in skeletal muscle of elderly people may reflect an anti-inflammatory response to the increased gene expression of IL-1␤ (118). IL-10 inhibits the proteolytic effects of IL-1␤ in muscle cells (149).…”

Section: Evidence For a Role Of Inflammation In Sarcopeniamentioning

confidence: 99%

Aging and its effects on inflammation in skeletal muscle at rest and following exercise-induced muscle injury

Peake

Gatta

Cameron‐Smith

2010

American Journal of Physiology-Regulatory, Integrative and Comp

160

136

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“…Moreover, TNF-␣ (39, 57, 62), IL-1␤ (29), and IL-2 can impair striated muscle function (50). However, apart from damaging the muscle, cytokines can augment the repair process (after injury) by enhancing the activation of macrophages (48,57), through promoting myoblast differentiation (TNF-␣ and IL-10) (11,46,49) or promoting myoblast proliferation on the initial phase of muscle regeneration (IL-6) (49). Moreover, IL-10 attenuates cytokine upregulation within the diaphragm of mice with Pseudomonas aeruginosa lung infection (14).…”

Section: Role Of Cytokinesmentioning

confidence: 99%

MAPKs and NF-κB differentially regulate cytokine expression in the diaphragm in response to resistive breathing: the role of oxidative stress

Sigala

Zacharatos²,

Toumpanakis

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Inspiratory resistive breathing (IRB) induces cytokine expression in the diaphragm. The mechanism of this cytokine induction remains elusive. The roles of MAPKs and NF-κB and the impact of oxidative stress in IRB-induced cytokine upregulation in the diaphragm were studied. Wistar rats were subjected to IRB (50% of maximal inspiratory pressure) via a two-way nonrebreathing valve for 1, 3, or 6 h. Additional groups of rats subjected to IRB for 6 h were randomly assigned to receive either solvent or N-acetyl-cysteine (NAC) or inhibitors of NF-κB (BAY-11–7082), ERK1/2 (PD98059), and P38 MAPK (SB203580) to study the effect of oxidative stress, NF-κB, and MAPKs in IRB-induced cytokine upregulation in the diaphragm. Quietly breathing animals served as controls. IRB upregulated cytokine (IL-6, TNF-α, IL-10, IL-2, IL-1β) protein levels in the diaphragm and resulted in increased activation of MAPKs (P38, ERK1/2) and NF-κB. Inhibition of NF-κB and ERK1/2 blunted the upregulation of all cytokines except that of IL-6, which was further increased. P38 inhibition attenuated all cytokine (including IL-6) upregulation. Both P38 and ERK1/2 inhibition decreased NF-κB/p65 subunit phosphorylation. NAC pretreatment blunted IRB-induced cytokine upregulation in the diaphragm and resulted in decreased ERK1/2, P38, and NF-κB/p65 phosphorylation. In conclusion, IRB-induced cytokine upregulation in the diaphragm is under the regulatory control of MAPKs and NF-κB. IL-6 is regulated differently from all other cytokines through a P38-dependent and NF-κB independent pathway. Oxidative stress is a stimulus for IRB-induced cytokine upregulation in the diaphragm.

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Prototypical anti-inflammatory cytokine IL-10 prevents loss of IGF-I-induced myogenin protein expression caused by IL-1β

Cited by 25 publications

References 56 publications

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Aging and its effects on inflammation in skeletal muscle at rest and following exercise-induced muscle injury

MAPKs and NF-κB differentially regulate cytokine expression in the diaphragm in response to resistive breathing: the role of oxidative stress

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