Interleukin-1β mediates endotoxin- and tumor necrosis factor α-induced RGS16 protein expression in cultured cardiac myocytes
Endotoxin (LPS)-induced cardiac failure is associated with an up-regulation of RGS16 protein expression and repression of phospholipase C activity in vivo. Since the release of pro-inflammatory cytokines plays an important role in mediating LPS-induced myocardial dysfunction, we examined the effect...
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| Hauptverfasser: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
18 October 2003
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| In: |
Naunyn-Schmiedeberg's archives of pharmacology
Year: 2003, Jahrgang: 368, Heft: 5, Pages: 360-365 |
| ISSN: | 1432-1912 |
| DOI: | 10.1007/s00210-003-0798-0 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00210-003-0798-0
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| Verfasserangaben: | Monica Patten, Sabine Stübe, Bryan Thoma, Thomas Wieland |
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| 245 | 1 | 0 | |a Interleukin-1β mediates endotoxin- and tumor necrosis factor α-induced RGS16 protein expression in cultured cardiac myocytes |c Monica Patten, Sabine Stübe, Bryan Thoma, Thomas Wieland |
| 246 | 3 | 3 | |a Interleukin-1 beta mediates endotoxin- and tumor necrosis factor alpha-induced RGS16 protein expression in cultured cardiac myocytes |
| 264 | 1 | |c 18 October 2003 | |
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| 520 | |a Endotoxin (LPS)-induced cardiac failure is associated with an up-regulation of RGS16 protein expression and repression of phospholipase C activity in vivo. Since the release of pro-inflammatory cytokines plays an important role in mediating LPS-induced myocardial dysfunction, we examined the effect of recombinant cytokines on the expression of RGS16 protein in neonatal cardiac myocytes. Myocytes in culture were treated with 50 ng/ml recombinant tumor necrosis factor alpha (TNFalpha), 2 ng/ml interleukin 1beta (IL-1beta), interleukin 6 (IL-6), interferon gamma (IFNgamma) or diluent (NaCl) for 24 h. Before stimulation with LPS (4 micro g/ml for 24 h) cells were treated with 200 ng/ml interleukin 1-receptor antagonist (IL-1ra), 500 ng/ml soluble TNF receptor (sTNFr), or NaCl for 1 h. Isolated membrane proteins were used for Western blot analysis. Cell-associated and secreted IL-1beta and TNFalpha protein content were determined in myocyte protein homogenates and cell culture supernatants by ELISA immunoblotting 3, 6, 24, 48 and 72 h after treatment with LPS. IL-1beta (1.75-fold) and TNFalpha (1.62-fold) but not IL-6 and IFNgamma induced RGS16 protein expression. LPS stimulated intracellular IL-1beta expression within 6 h (847.1+/-172.9 pg/3x10(6) cells) followed by an increase in extracellular secretion up to 70.8+/-8.1 pg/3x10(6) cells after 48 h. In contrast, intracellular protein concentrations of TNFalpha were almost not detectable (0.03+/-0.01 pg/3x10(6) cells), but extracellular secretion was induced by LPS with a maximum at 6 h (653.9+/-36.3 pg/3x10(6) cells). The LPS-induced increase in RGS16 (1.6-fold) was blunted by IL-1ra but not by TNFalpha scavenging. Interestingly, both, the IL-1beta- and TNFalpha-effect could be blocked by IL-1ra, indicating that also the TNFalpha-induced RGS16 expression is mediated by IL-1. We therefore conclude that LPS induces RGS16 protein expression by activation of the cytokine IL-1beta in cardiac myocytes. Our data substantiate the role of IL-1beta as an important mediator in LPS-induced cardiac failure. | ||
| 650 | 4 | |a Animals | |
| 650 | 4 | |a Animals, Newborn | |
| 650 | 4 | |a Blotting, Western | |
| 650 | 4 | |a Cells, Cultured | |
| 650 | 4 | |a Interferon-gamma | |
| 650 | 4 | |a Interleukin-1 | |
| 650 | 4 | |a Interleukin-6 | |
| 650 | 4 | |a Lipopolysaccharides | |
| 650 | 4 | |a Myocytes, Cardiac | |
| 650 | 4 | |a Protein Biosynthesis | |
| 650 | 4 | |a Proteins | |
| 650 | 4 | |a Rats | |
| 650 | 4 | |a Receptors, Interleukin-1 | |
| 650 | 4 | |a Recombinant Proteins | |
| 650 | 4 | |a RGS Proteins | |
| 650 | 4 | |a Time Factors | |
| 650 | 4 | |a Tumor Necrosis Factor-alpha | |
| 700 | 1 | |a Stübe, Sabine |e VerfasserIn |4 aut | |
| 700 | 1 | |a Thoma, Bryan Robert |e VerfasserIn |0 (DE-588)137928831 |0 (DE-627)598159134 |0 (DE-576)305876953 |4 aut | |
| 700 | 1 | |a Wieland, Thomas |d 1960-2025 |e VerfasserIn |0 (DE-588)1033445908 |0 (DE-627)741233215 |0 (DE-576)381043339 |4 aut | |
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