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Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo

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Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo. / Patten, M; Krämer, E; Bünemann, J; Wenck, C; Thoenes, M; Wieland, T; Long, C.

In: PFLUG ARCH EUR J PHY, Vol. 442, No. 6, 09.2001, p. 920-927.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Patten, M, Krämer, E, Bünemann, J, Wenck, C, Thoenes, M, Wieland, T & Long, C 2001, 'Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo', PFLUG ARCH EUR J PHY, vol. 442, no. 6, pp. 920-927. https://doi.org/10.1007/s004240100612

APA

Patten, M., Krämer, E., Bünemann, J., Wenck, C., Thoenes, M., Wieland, T., & Long, C. (2001). Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo. PFLUG ARCH EUR J PHY, 442(6), 920-927. https://doi.org/10.1007/s004240100612

Vancouver

Patten M, Krämer E, Bünemann J, Wenck C, Thoenes M, Wieland T et al. Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo. PFLUG ARCH EUR J PHY. 2001 Sep;442(6):920-927. https://doi.org/10.1007/s004240100612

Bibtex

@article{1384ccca6983431ab246c35092b4a4a2,
title = "Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo",
abstract = "Release of bacterial endotoxin and cytokines induce cardiac failure during sepsis. We investigated the direct effects of E. coli endotoxin (lipopolysaccharide, LPS) and cytokines induced by LPS on the cardiac myocyte gene program. For in vivo-experiments adult Wistar rats were given 600 microg/day LPS i.v. for 24 h or 7 days. In addition, cultured adult rat cardiac myocytes were treated with LPS, interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNFalpha), interferon-gamma (IFNgamma) or IL-6 for 24 h. mRNA expression was evaluated for cardiac-alpha-actin (cAct), skeletal-alpha-actin (skAct), beta- and alpha-myosin heavy chain (MHC). LPS induced betaMHC-mRNA 3.6-fold and repressed alphaMHC 2.7-fold and cAct 2.5-fold after 24 h in vivo. Up-regulation of betaMHC (3-fold) and repression of cAct (2.5-fold) were still observed after 7 days LPS infusion, whereas alphaMHC-mRNA levels had returned to normal. At the protein level, increased expression of betaMHC by LPS treatment occurred already after 24 h and was maintained thereafter. LPS had no influence on skAct-mRNA. Similar changes in contractile protein mRNA expression were observed in LPS-treated cardiomyocytes in culture, whereas the tested cytokines either activated (IL-1beta, IFNgamma) or repressed (TNFalpha, IL-6) both MHC-isoforms and cAct. In conclusion, LPS and proinflammatory cytokines induce changes in contractile protein expression that may contribute to the acute heart failure observed during endotoxaemia.",
keywords = "Actins/genetics, Animals, Cells, Cultured, Contractile Proteins/genetics, Cytokines/genetics, Escherichia coli, Gene Expression/drug effects, Interferon-gamma/pharmacology, Interleukin-1/pharmacology, Interleukin-6/pharmacology, Lipopolysaccharides/pharmacology, Myocardium/metabolism, Myosin Heavy Chains/genetics, RNA, Messenger/analysis, Rats, Rats, Wistar, Time Factors, Tumor Necrosis Factor-alpha/pharmacology",
author = "M Patten and E Kr{\"a}mer and J B{\"u}nemann and C Wenck and M Thoenes and T Wieland and C Long",
year = "2001",
month = sep,
doi = "10.1007/s004240100612",
language = "English",
volume = "442",
pages = "920--927",
journal = "PFLUG ARCH EUR J PHY",
issn = "0031-6768",
publisher = "Springer",
number = "6",

}

RIS

TY - JOUR

T1 - Endotoxin and cytokines alter contractile protein expression in cardiac myocytes in vivo

AU - Patten, M

AU - Krämer, E

AU - Bünemann, J

AU - Wenck, C

AU - Thoenes, M

AU - Wieland, T

AU - Long, C

PY - 2001/9

Y1 - 2001/9

N2 - Release of bacterial endotoxin and cytokines induce cardiac failure during sepsis. We investigated the direct effects of E. coli endotoxin (lipopolysaccharide, LPS) and cytokines induced by LPS on the cardiac myocyte gene program. For in vivo-experiments adult Wistar rats were given 600 microg/day LPS i.v. for 24 h or 7 days. In addition, cultured adult rat cardiac myocytes were treated with LPS, interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNFalpha), interferon-gamma (IFNgamma) or IL-6 for 24 h. mRNA expression was evaluated for cardiac-alpha-actin (cAct), skeletal-alpha-actin (skAct), beta- and alpha-myosin heavy chain (MHC). LPS induced betaMHC-mRNA 3.6-fold and repressed alphaMHC 2.7-fold and cAct 2.5-fold after 24 h in vivo. Up-regulation of betaMHC (3-fold) and repression of cAct (2.5-fold) were still observed after 7 days LPS infusion, whereas alphaMHC-mRNA levels had returned to normal. At the protein level, increased expression of betaMHC by LPS treatment occurred already after 24 h and was maintained thereafter. LPS had no influence on skAct-mRNA. Similar changes in contractile protein mRNA expression were observed in LPS-treated cardiomyocytes in culture, whereas the tested cytokines either activated (IL-1beta, IFNgamma) or repressed (TNFalpha, IL-6) both MHC-isoforms and cAct. In conclusion, LPS and proinflammatory cytokines induce changes in contractile protein expression that may contribute to the acute heart failure observed during endotoxaemia.

AB - Release of bacterial endotoxin and cytokines induce cardiac failure during sepsis. We investigated the direct effects of E. coli endotoxin (lipopolysaccharide, LPS) and cytokines induced by LPS on the cardiac myocyte gene program. For in vivo-experiments adult Wistar rats were given 600 microg/day LPS i.v. for 24 h or 7 days. In addition, cultured adult rat cardiac myocytes were treated with LPS, interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNFalpha), interferon-gamma (IFNgamma) or IL-6 for 24 h. mRNA expression was evaluated for cardiac-alpha-actin (cAct), skeletal-alpha-actin (skAct), beta- and alpha-myosin heavy chain (MHC). LPS induced betaMHC-mRNA 3.6-fold and repressed alphaMHC 2.7-fold and cAct 2.5-fold after 24 h in vivo. Up-regulation of betaMHC (3-fold) and repression of cAct (2.5-fold) were still observed after 7 days LPS infusion, whereas alphaMHC-mRNA levels had returned to normal. At the protein level, increased expression of betaMHC by LPS treatment occurred already after 24 h and was maintained thereafter. LPS had no influence on skAct-mRNA. Similar changes in contractile protein mRNA expression were observed in LPS-treated cardiomyocytes in culture, whereas the tested cytokines either activated (IL-1beta, IFNgamma) or repressed (TNFalpha, IL-6) both MHC-isoforms and cAct. In conclusion, LPS and proinflammatory cytokines induce changes in contractile protein expression that may contribute to the acute heart failure observed during endotoxaemia.

KW - Actins/genetics

KW - Animals

KW - Cells, Cultured

KW - Contractile Proteins/genetics

KW - Cytokines/genetics

KW - Escherichia coli

KW - Gene Expression/drug effects

KW - Interferon-gamma/pharmacology

KW - Interleukin-1/pharmacology

KW - Interleukin-6/pharmacology

KW - Lipopolysaccharides/pharmacology

KW - Myocardium/metabolism

KW - Myosin Heavy Chains/genetics

KW - RNA, Messenger/analysis

KW - Rats

KW - Rats, Wistar

KW - Time Factors

KW - Tumor Necrosis Factor-alpha/pharmacology

U2 - 10.1007/s004240100612

DO - 10.1007/s004240100612

M3 - SCORING: Journal article

C2 - 11680626

VL - 442

SP - 920

EP - 927

JO - PFLUG ARCH EUR J PHY

JF - PFLUG ARCH EUR J PHY

SN - 0031-6768

IS - 6

ER -