eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
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vol. 15
Experimental research

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

Magdalena Dziemidowicz
Tomasz A. Bonda
Siergiej Litvinovich
Andrzej Taranta
Maria M. Winnicka
Karol A. Kamiński

Arch Med Sci 2019; 15 (6): 1565–1575
Online publish date: 2019/11/03
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Inflammatory 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 methods
Experiments 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.

Chronic 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).

IL-6 plays an important role in regulating the activation of MAPK pathways in the mouse myocardium in response to chronic β-adrenergic stimulation.


interleukin-6, ERK, signal transduction, adrenergic stimulation, heart, isoproterenol

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