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, Jahrgang 442, Nr. 6, 09.2001, S. 920-927.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -