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Updated: Aug 14, 2026
Isolation and Physiological Analysis of Mouse Cardiomyocytes
Published on: September 7, 2014
Cytokines induce stress protein formation in cultured cardiac myocytes
I Löw-Friedrich1, D Weisensee, P Mitrou
1Department of Nephrology, Hospital of the Johann Wolfgang Goethe University, Frankfurt am Main, FRG.
Insights
Cytokines like interleukins and tumor necrosis factor directly impact heart cells, causing arrhythmias and altering protein synthesis. These immune mediators may activate protective mechanisms within cardiac myocytes.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cellular Stress Response
Background:
- Severe cardiac impairment in diseases like sepsis and uremia correlates with increased cytokine release.
- Cytokines are immune mediators with potential toxic effects on myocardial cells.
Purpose of the Study:
- To investigate the direct effects of cytokines on cardiac myocyte contractility.
- To examine the de novo formation of stress proteins in heart cells exposed to cytokines.
Main Methods:
- Cultured heart cells were exposed to various cytokines.
- Cardiac myocyte contractility was assessed.
- De novo synthesis of stress proteins was analyzed.
Main Results:
- All tested cytokines induced concentration-dependent arrhythmias and cessation of spontaneous contractions.
- Interleukin-2, IL-3, IL-6, and tumor necrosis factor stimulated a 30 kD stress protein.
- Interleukin-1 induced two additional 70 kD stress proteins.
Conclusions:
- Cytokines directly interfere with myocytes and myocardial protein formation.
- Cytokines may activate protective mechanisms in cardiac myocytes by inducing stress proteins, enhancing resistance to subsequent challenges.
Abstract:
Diseases accompanied by severe cardiac impairment like sepsis and chronic uremia are frequently linked to an increase in cytokine release. In order to investigate possible toxic effects of the immune mediators on myocardial cells, we studied the contractility of cardiac myocytes and the de novo formation of stress proteins in cultured heart cells under cytokine exposition. All cytokines investigated induce, concentration-dependently, arrhythmias and cessation of spontaneous contractions. Interleukin(IL)-2, IL-3, IL-6, and tumor necrosis factor (TNF) stimulate the synthesis of a 30 kD stress protein in heart cells, whereas IL-1 additionally evokes two proteins of the 70 kD family. These findings confirm a direct interference of the interleukins and TNF with myocytes and, especially, myocardial protein formation. As the induction of stress proteins makes cells more resistant towards a subsequent challenge, the cytokines are possibly involved in the activation of cell protecting mechanisms in cardiac myocytes.
