scholarly journals Recombinant human interleukin-6 (IL-6/BSF-2/HSF) regulates the synthesis of acute phase proteins in human hepatocytes

FEBS Letters ◽  
1988 ◽  
Vol 232 (2) ◽  
pp. 347-350 ◽  
Author(s):  
José V. Castell ◽  
Maria J. Gómez-Lechón ◽  
Martina David ◽  
Toshio Hirano ◽  
Tadamitsu Kishimoto ◽  
...  
Keyword(s):  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Human Hepatocytes

scholarly journals MicroRNA-18a Enhances the Interleukin-6-mediated Production of the Acute-phase Proteins Fibrinogen and Haptoglobin in Human Hepatocytes

2011 ◽  
Vol 286 (46) ◽  
pp. 40142-40150 ◽  
Author(s):  
Matthias Brock ◽  
Michelle Trenkmann ◽  
Renate E. Gay ◽  
Steffen Gay ◽  
Rudolf Speich ◽  
...  
Keyword(s):  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Human Hepatocytes

Acute Phase Proteins and Interleukin?6 Serum Levels in Patients with Chronic Arterial Occlusion

2006 ◽  
Vol 762 (1) ◽  
pp. 493-495 ◽  
Author(s):  
WACLAW MAJEWSKI ◽  
RYSZARD STANISZEWSKI ◽  
ARTUR SLUPIANEK ◽  
ALEKSANDER GORNY ◽  
ANDRZEJ MACKIEWICZ
Keyword(s):  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Arterial Occlusion ◽  
Serum Levels ◽  
Chronic Arterial Occlusion

Synergistic action of interleukin-6 and glucocorticoids is mediated by the interleukin-6 response element of the rat alpha 2 macroglobulin gene

1992 ◽  
Vol 12 (5) ◽  
pp. 2282-2294
Author(s):  
G M Hocke ◽  
D Barry ◽  
G H Fey
Keyword(s):  
Dna Binding ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Binding Proteins ◽  
Nuclear Dna ◽  
Acute Phase Proteins ◽  
Dna Binding Proteins ◽  
Human Hepatoma Cells ◽  
Response Element ◽  
Multiple Copies

One class of genes coding for the acute-phase proteins (acute-phase genes) is induced by interleukin 6 (IL-6) through the human transcription factor NF-IL-6 and its rat homolog IL-6-DBP/LAP. A second class, represented by the rat alpha 2 macroglobulin gene, utilizes a different IL-6 response element (IL-6-RE) and different DNA-binding proteins interacting with this element, the so-called IL-6-RE binding proteins (IL-6 RE-BPs). Human Hep3B and HepG2 hepatoma, U266 myeloma, and CESS lymphoblastoid cells contain IL-6 RE-BPs that form complexes, with the IL-6-RE, with gel mobilities indistinguishable from those of the corresponding complexes of rat liver cells. The ability to form these complexes was induced by IL-6 in human hepatoma cells with a maximum reached after 4 h and required ongoing protein synthesis. Multiple copies of an 18-bp element containing the IL-6-RE core were sufficient to confer both induction by IL-6 and a synergistic induction by IL-6 plus glucocorticoids to minimal promoters. The synergism was blocked by the receptor antagonist RU486 and thus was dependent on the glucocorticoid receptor (GR). However, the 18-bp element contained no consensus GR-binding site, and recombinant GR did not bind at this sequence. Therefore, the synergism was probably achieved by an indirect effect of a glucocorticoid-activated intermediate gene on the IL-6 RE-BPs. The rat IL-6 RE-BP had a molecular weight of 102 +/- 10 kDa and was thus distinct from NF-IL-6 and IL-6-DBP/LAP. Therefore, IL-6 must activate two different classes of liver acute-phase genes through at least two different nuclear DNA-binding proteins: NF-IL-6/IL-6-DBP/LAP and the IL-6 RE-BP.

scholarly journals Pathogenic significance of interleukin-6 (IL-6/BSF-2) in Castleman's disease

Blood ◽  
1989 ◽  
Vol 74 (4) ◽  
pp. 1360-1367 ◽  
Author(s):  
K Yoshizaki ◽  
T Matsuda ◽  
N Nishimoto ◽  
T Kuritani ◽  
L Taeho ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Nodes ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Castleman’S Disease ◽  
Germinal Centers ◽  
Surgical Removal ◽  
Castleman's Disease ◽  
Lymph Node Hyperplasia

Abstract Castleman's disease is a syndrome consisting of giant lymph node hyperplasia with plasma cell infiltration, fever, anemia, hypergammaglobulinemia, and an increase in the plasma level of acute phase proteins. It has been reported that clinical abnormalities disappear after the resection of the affected lymph nodes, suggesting that products of lymph nodes may cause such clinical abnormalities. Interleukin-6 (IL-6) is a cytokine inducing B-cell differentiation to immunoglobulin-producing cells and regulating biosynthesis of acute phase proteins. This report demonstrates that the germinal centers of hyperplastic lymph nodes of patients with Castleman's disease produce large quantities of IL-6 without any significant production of other cytokines. In a patient with a solitary hyperplastic lymph node, clinical improvement and decrease in serum IL-6 were observed following surgical removal of the involved lymph node. There was a correlation between serum IL-6 level, lymph node hyperplasia, hypergammaglobulinemia, increased level of acute phase proteins, and clinical abnormalities. The findings in this report indicate that the generation of IL-6 by B cells in germinal centers of hyperplastic lymph nodes of Castleman's disease may be the key element responsible for the variety of clinical symptoms in this disease.

scholarly journals Okadaic acid, an inhibitor of protein phosphatases 1 and 2A, inhibits induction of acute-phase proteins by interleukin-6 alone or in combination with interleukin-1 in human hepatoma cell lines

1992 ◽  
Vol 284 (3) ◽  
pp. 645-648 ◽  
Author(s):  
M K Ganapathi
Keyword(s):  
Acute Phase ◽  
Okadaic Acid ◽  
Interleukin 6 ◽  
Acute Phase Proteins ◽  
Protein Phosphatases ◽  
Hepatoma Cell ◽  
Interleukin 1 ◽  
Dependent Manner ◽  
Amyloid A ◽  
20 Nm

Okadaic acid (OA), a specific inhibitor of protein phosphatases 1 and 2A, inhibited in a dose-dependent manner (5-20 nM) the induction of C-reactive protein (CRP), serum amyloid A (SAA) and fibrinogen by interleukin-6 (IL-6) plus interleukin-1 (IL-1), and of fibrinogen by IL-6 alone, in Hep 3B cells. Induction of alpha 1-proteinase inhibitor (alpha 1-PI) by IL-6 plus IL-1 or IL-6 alone was not significantly affected by OA up to concentrations of 20 nM, above which concentration OA was toxic in Hep 3B cells. OA also inhibited the induction of CRP, fibrinogen and alpha 1-PI by IL-6 in the NPLC/PRF/5 cell line, albeit at a higher concentration (80 nM). These results suggest that the signal transduction mechanisms regulating induction of acute-phase proteins by IL-6, either alone or in combination with IL-1, are mediated by activation of protein phosphatases 1 and/or 2A.

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