scholarly journals Serum amyloid A3 expression is stimulated by dexamethasone and interleukin-6 in 3T3-L1 adipocytes

2004 ◽  
Vol 183 (3) ◽  
pp. 561-567 ◽  
Author(s):  
Mathias Fasshauer ◽  
Johannes Klein ◽  
Susan Kralisch ◽  
Margit Klier ◽  
Ulrike Lossner ◽  
...  

A chronic increase in systemic levels of acute-phase reactants contributes to the development of insulin resistance and associated disorders such as cardiovascular disease. Recently, serum amyloid A3 (SAA3) has been characterized as an adipocyte-secreted acute-phase reactant, expression of which is dramatically increased in insulin resistance and obesity. To further clarify expression and regulation of this adipocytokine in fat, SAA3 mRNA was measured by quantitative real-time reverse transcriptase PCR during differentiation of 3T3-L1 adipocytes and after treatment with various hormones known to induce insulin resistance and contribute to atherosclerosis. SAA3 mRNA was dramatically induced up to 77-fold during differentiation of 3T3-L1 preadipocytes. Furthermore, 100 nM dexamethasone and 30 ng/ml interleukin (IL)-6 induced SAA3 mRNA by up to 11- and 4.8-fold, respectively, in a time-dependent fashion with significant stimulation observed at concentrations as low as 10 nM dexamethasone and 1 ng/ml IL-6. In contrast, insulin, isoproterenol and growth hormone did not influence SAA3 synthesis. Inhibitor studies suggested that the positive effect of IL-6 on SAA3 expression is at least in part mediated by Janus kinase 2. Taken together, our results show a differential regulation of SAA3 by glucocorticoids and IL-6 supporting an integrative role of this acute-phase reactant in the pathogenesis of insulin resistance and its link to obesity and cardiovascular disease.

2009 ◽  
Vol 28 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Irena Kafeđiska ◽  
Dejan Spasovski ◽  
Todor Gruev ◽  
Mane Grličkov ◽  
Kočo Cakalaroski ◽  
...  

Association Between Osteoarticular Scores and Acute Phase Reactant Levels in Rheumatoid Arthritis The aim of this prospective control study was a quantitative evaluation of the activity of rheumatoid arthritis (RA) in certain time intervals, using articular indexes (set of 28 sensitive and 28 swollen joints), laboratory parameters (Hb, Hct, Er, Le and Plt) and acute phase reactants (ESR, RF, CRP); to determine which of the acute phase reactants is the most useful biochemical marker for the evaluation of disease activity in RA; to quantify the therapeutical and laboratory differences in certain time intervals in the group with and without immunomodulatory therapy with Methotrexate. Sixty patients with RA were included, 27 of who were treated with non-steroid antiinflammatory drugs (NSAIDs) and Methotrexate (MTX). The control group consisted of 33 patients treated only with NSAIDs because of irregular controls. In the first group of patients the disease activity was estimated at four time intervals, and in the control group of patients at three time intervals following the scores of the articular indexes, blood cell counts, ESR and CRP in every patient. In the first group of patients decreased activity of RA was found upon every following control with a consecutive decrease in mean values of the scores of articular indexes with statistically significant differences at the four time intervals. Considering laboratory parameters, there were statistically significant differences in the mean values of Hb, Er, Plt, ESR, (p=0.0462, p=0.0076, p= 0.0058, p= 0.0003). Mean values of CRP did not show statistically significant differences, but the number of patients who were CRP negative increased (there were great standard deviations). In the group of patients treated only with NSAIDs, there were statistically significant differences in the mean values of the scores of articular indexes with an increse at every following control (in favour of progression of the disease). There were no statistically significant differences considering blood cell counts, ESR and CRP (in favour of permanently active disease). In conclusion, CRP is the most useful marker for the prospective follow-up of patients with RA.


1987 ◽  
Author(s):  
K W Prasse ◽  
J N Moore ◽  
A Duncan

Equine Colic Syndrome is a disease of horses whose complications include laminatis.This term describes a situation where microvascular damage to the hoof causes degeneration of the interphalangeal laminae,leading to lameness. Vascular studies have suggested that microthrombosis involving the delicate vessels in the hoof,coupled with changes in the platelet count, coagulation factors & elevated FDP's implicate DIC as a potential etiology. Limited test capability in the horse has limited further evaluation of this hypothesis. We have developed an assay for equine protein C activity,our normal range being 70-60% (Mean+/- 2SD). We studied 12 horses with the disease for 5 consecutive days,drawing 1 blood sample per day. Our expectation was that protein C levels would decrease.if DIC was significant,as would be expected in humans. No significant decrease was noted in any horse. However there was a significant increase in the protein C levels beyond the upper limit of the normal range in 10 of the 12 horses by the third day. Five of the 10 horses maintained this elevation beyond the 5th day. Thus protein C changes were more consistent with an acute phase reactant response,rather than reflecting the decrease we anicipated,if the equine DIC parallels human DIC. We are measuring other acute phase reactants to see if equine protein C parallels those. Since our assay is still being evaluated,more data needs to be obtained in this and other equine disease states before any definative role for protein C in equine pathology can be determined. In our laminitis horses,we are devolping assays for antithrombin III and plasminogen which should allow us to evaluate the disease state more completley for any involement of elements of intravascular thrombosis and fibrinolysis in the equine colic syndrome.


2008 ◽  
Vol 32 (10) ◽  
pp. 1160-1169 ◽  
Author(s):  
Franz Villarroel ◽  
Alin Casado ◽  
Jorge Vásquez ◽  
Ella Matamala ◽  
Bruno Araneda ◽  
...  

Nature ◽  
1979 ◽  
Vol 278 (5701) ◽  
pp. 259-261 ◽  
Author(s):  
M. B. PEPYS ◽  
MARILYN BALTZ ◽  
K. GOMER ◽  
A. J. S. DAVIES ◽  
M. DOENHOFF

Amyloidosis ◽  
1986 ◽  
pp. 87-97 ◽  
Author(s):  
Shunsuke Migita ◽  
Shigeru Hashimototo ◽  
Haruo Hisazumi ◽  
Mine Harada ◽  
Hiroaki Okabe

2019 ◽  
pp. 25-80 ◽  
Author(s):  
Yan Zhang ◽  
Jie Zhang ◽  
Huiming Sheng ◽  
Haichuan Li ◽  
Rongfang Wang

1982 ◽  
Vol 155 (2) ◽  
pp. 345-357 ◽  
Author(s):  
I Hara ◽  
S Izui ◽  
F J Dixon

A single intraperitoneal injection of bacterial lipopolysaccharide (LPS) or its lipid A component induced high levels of glycoprotein, gp70, in sera of several strains of mice within 24 h. This serum gp70 response induced by LPS was independent of the activation of B cells and the presence of T cells. However, serological and immunohistochemical studies demonstrated the production of gp70 by hepatic parenchymal cells and its subsequent release into the circulating blood. The expression of gp70 in the serum was enhanced not only by LPS but also other inducers of acute phase reactants (APR) such as turpentine oil or polyriboinosinic-polyribocytidylic acid. Further, the serum gp70 response was kinetically identical to those of APR. These results strongly suggest that (a) the liver may be the major source for serum gp70, (b) serum gp70 behaves like an APR, (c) its expression may be controlled by a mechanism similar to that for other APR, and (d) this glycoprotein apparently behaves as a normal host constituent and not a product of a viral genome.


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