Increased expression of C-reactive protein gene in inflamed gingival tissues could be derived from endothelial cells stimulated with interleukin-6

2011 ◽  
Vol 56 (11) ◽  
pp. 1312-1318 ◽  
Author(s):  
Tomoki Maekawa ◽  
Koichi Tabeta ◽  
Keiko Kajita-Okui ◽  
Takako Nakajima ◽  
Kazuhisa Yamazaki
Keyword(s):  
Endothelial Cells ◽  
Interleukin 6 ◽  
Protein Gene ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals STAT3 Participates in Transcriptional Activation of the C-reactive Protein Gene by Interleukin-6

1996 ◽  
Vol 271 (16) ◽  
pp. 9503-9509 ◽  
Author(s):  
Dongxiao Zhang ◽  
Ming Sun ◽  
David Samols ◽  
Irving Kushner
Keyword(s):  
Transcriptional Activation ◽  
Interleukin 6 ◽  
Protein Gene ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Dual control of C-reactive protein gene expression by interleukin-1 and interleukin-6.

1989 ◽  
Vol 8 (12) ◽  
pp. 3773-3779 ◽  
Author(s):  
U. Ganter ◽  
R. Arcone ◽  
C. Toniatti ◽  
G. Morrone ◽  
G. Ciliberto
Keyword(s):  
Gene Expression ◽  
Interleukin 6 ◽  
Protein Gene ◽  
Interleukin 1 ◽  
Dual Control ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Interleukin-6-dependent and -independent regulation of the human C-reactive protein gene

1997 ◽  
Vol 327 (2) ◽  
pp. 425-429 ◽  
Author(s):  
Birgit WEINHOLD ◽  
Ulrich RÜTHER
Keyword(s):  
Transgenic Mice ◽  
Interleukin 6 ◽  
Protein Gene ◽  
Model System ◽  
Oncostatin M ◽  
Leukaemia Inhibitory Factor ◽  
C Reactive Protein ◽  
Cytokine Network ◽  
Reactive Protein ◽  
Novel Model

We have investigated the function of different mediators of the regulation of the human C-reactive protein (hCRP) gene in transgenic mice. hCRP was induced by lipopolysaccharide and wounding in interleukin-6 (IL-6) +/+ mice, but not in IL-6 -/- mice. This finding suggested that IL-6 is necessary for the induction of hCRP. However, injection of IL-6 did not induce the hCRP gene. Thus, the induction of hCRP by IL-6 seems to require an additional cofactor. Therefore, we screened different cytokines for their activity in IL-6 +/+ and IL-6 -/- mice. Surprisingly, interleukin-1β, as well as oncostatin M or leukaemia inhibitory factor, led to an induction of hCRP in both genetic backgrounds. These results indicate an IL-6-dependent and -independent regulation of hCRP. These hCRP transgenic mice therefore represent a novel model system for defining the cytokine network involved in the regulation of acute-phase genes during the course of inflammation.

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