Interleukin 6 is not necessary for STAT3 phosphorylation and myocardial hypertrophy following short term beta-adrenergic stimulation

Kamiński, Karol; Dziemidowicz, Magdalena; Литвинович, С. Н.; Bonda, Tomasz A.; Ptaszynska, K; Kożuch, Marcin; Taranta, Andrzej; Musiał, W; Winnicka, Maria M.

doi:10.2478/v10039-011-0059-2

Cited by 3 publications

(3 citation statements)

References 22 publications

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“…Previous studies have shown that the lack of IL-6 does not affect the activation of STAT3 and ERK1/2 after a short bout of adrenergic stimulation in mouse [29]. In the present study chronic ISO administration caused an increase of phosphorylation of ERK kinases while having no effect on STAT3 activation.…”

Section: Discussionsupporting

confidence: 49%

“…Excessive stimulation of β-adrenergic receptors upregulates expression of IL-6 in the cardiomyocytes and cardiac fibroblasts [26–28], so at least some overlapping activities of both these factors could be expected. Additionally, in our previous study short term β-adrenergic stimulation with isoproterenol (ISO) was able to induce STAT3 phosphorylation independently from IL-6 [29], supporting the hypothesis assuming the interplay between IL-6- and β-adrenergic-dependent signaling pathways. However, this relationship is not conclusively determined and its better understanding may reveal new mechanisms involved in myocardial remodeling and secondary cardiac injury in the course of chronic heart failure.…”

Section: Introductionmentioning

confidence: 56%

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The role of interleukin-6 in intracellular signal transduction after chronic β-adrenergic stimulation in mouse myocardium

Dziemidowicz¹,

Bonda²,

Litvinovich³

et al. 2019

aoms

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IntroductionInflammatory mediators play an important role in development and progression of cardiovascular disease. Both adrenergic stimulation and high levels of interleukin-6 (IL-6) indicate an unfavorable outcome in patients with myocardial infarction or heart failure. Understanding the interaction between β-adrenergic stimulation and IL-6 in the myocardium may contribute to developing more effective treatments. The aim of this study was to verify the role of IL-6 in the effects of β-adrenergic stimulation in activating selected intracellular signaling pathways in mouse myocardium.Material and methodsExperiments were performed on 12-week-old male mice: 16 C57BL/6JIL6‑/‑TMKopf (IL-6 KO) and 17 C57BL/6J (WT). Animals received intraperitoneal injections of isoproterenol (ISO, 50 mg/kg) or placebo (0.9% NaCl) once a day for 16 days. The phosphorylation of STAT3 (signal transducer and activator of transcription 3), ERK1/2 (extracellular-regulated kinases 1/2), Akt1/2/3, p-38, c-Raf and expression of SOCS3 (suppressor of cytokine signaling 3), PIAS1/3 (protein inhibitors of activated STAT) was assessed by western blotting in the myocardium 24 h after the last injection. Evaluation of gene expression downstream of these pathways was performed by real-time PCR.ResultsChronic ISO treatment leads to increased fibrosis of the myocardium in mice lacking IL-6, which is accompanied by increased activity of ERK1/2, p38 and reduced expression of SOCS3. Administration of ISO in IL-6 KO animals intensified gene expression of proteins activated by MAPK/ERK (myc; CEBPB; BMP4; Fasn; Tank), while it reduced expression of genes repressed by ERK 1/2 (Wisp1, Wnt1).ConclusionsIL-6 plays an important role in regulating the activation of MAPK pathways in the mouse myocardium in response to chronic β-adrenergic stimulation.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 56%

The role of interleukin-6 in intracellular signal transduction after chronic β-adrenergic stimulation in mouse myocardium

Dziemidowicz¹,

Bonda²,

Litvinovich³

et al. 2019

aoms

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show abstract

“…Thus, the observed metabolic differences must be exerted through other pathways. In addition, a variety of other cytokines and hormones have been reported to trigger the STAT3 signaling pathway [ 51 , 52 ] and any of these, or non-muscle derived IL-6 may be responsible for the observed STAT3 pathway inductions and explain why this response was also present in IL-6 MKO mice.…”

Section: Discussionmentioning

confidence: 99%

Lack of Skeletal Muscle IL-6 Affects Pyruvate Dehydrogenase Activity at Rest and during Prolonged Exercise

et al. 2016

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Pyruvate dehydrogenase (PDH) plays a key role in the regulation of skeletal muscle substrate utilization. IL-6 is produced in skeletal muscle during exercise in a duration dependent manner and has been reported to increase whole body fatty acid oxidation, muscle glucose uptake and decrease PDHa activity in skeletal muscle of fed mice. The aim of the present study was to examine whether muscle IL-6 contributes to exercise-induced PDH regulation in skeletal muscle. Skeletal muscle-specific IL-6 knockout (IL-6 MKO) mice and floxed littermate controls (control) completed a single bout of treadmill exercise for 10, 60 or 120 min, with rested mice of each genotype serving as basal controls. The respiratory exchange ratio (RER) was overall higher (P<0.05) in IL-6 MKO than control mice during the 120 min of treadmill exercise, while RER decreased during exercise independent of genotype. AMPK and ACC phosphorylation also increased with exercise independent of genotype. PDHa activity was in control mice higher (P<0.05) at 10 and 60 min of exercise than at rest but remained unchanged in IL-6 MKO mice. In addition, PDHa activity was higher (P<0.05) in IL-6 MKO than control mice at rest and 60 min of exercise. Neither PDH phosphorylation nor acetylation could explain the genotype differences in PDHa activity. Together, this provides evidence that skeletal muscle IL-6 contributes to the regulation of PDH at rest and during prolonged exercise and suggests that muscle IL-6 normally dampens carbohydrate utilization during prolonged exercise via effects on PDH.

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IL-6/gp130/STAT3 signaling contributed to the activation of the PERK arm of the unfolded protein response in response to chronic β-adrenergic stimulation

Men,

Guo,

Cao

et al. 2023

Free Radical Biology and Medicine

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Interleukin 6 is not necessary for STAT3 phosphorylation and myocardial hypertrophy following short term beta-adrenergic stimulation

Cited by 3 publications

References 22 publications

The role of interleukin-6 in intracellular signal transduction after chronic β-adrenergic stimulation in mouse myocardium

The role of interleukin-6 in intracellular signal transduction after chronic β-adrenergic stimulation in mouse myocardium

Lack of Skeletal Muscle IL-6 Affects Pyruvate Dehydrogenase Activity at Rest and during Prolonged Exercise

IL-6/gp130/STAT3 signaling contributed to the activation of the PERK arm of the unfolded protein response in response to chronic β-adrenergic stimulation

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