The Acute Phase Protein α1-Acid Glycoprotein: A Model for Altered Glycosylation During Diseases

2007 ◽  
Vol 8 (1) ◽  
pp. 91-108 ◽  
Author(s):  
Fabrizio Ceciliani ◽  
Vanessa Pocacqua
1992 ◽  
Vol 262 (5) ◽  
pp. R786-R793 ◽  
Author(s):  
R. J. Sharma ◽  
D. C. Macallan ◽  
P. Sedgwick ◽  
D. G. Remick ◽  
G. E. Griffin

The kinetics of cytokine release and acute-phase protein gene expression in liver were investigated in rats receiving a single intraperitoneal bolus dose of Escherichia coli lipopolysaccharide (LPS). Transient elevation of plasma tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected. Hepatic messenger RNAs for two acute-phase proteins, alpha 1-acid glycoprotein and alpha 2-macroglobulin, were measured by Northern blotting and were found to increase to a maximum at 24 h, returning to normal by 72 h; plasma concentrations showed a slower but more sustained rise. For albumin, hepatic mRNA was reduced, being minimum at 24 h with a similar but more prolonged fall in plasma concentration. Pretreatment of rats with TNF-alpha monoclonal antibody 4 h before LPS ameliorated weight loss and anorexia, partially suppressed the rise in IL-6 and reduced the increase in hepatic mRNA and plasma concentrations of alpha 1-acid glycoprotein and alpha 2-macroglobulin. For albumin, however, such pretreatment had no effect on the fall in either hepatic mRNA or plasma concentration. Thus we have defined an in vivo role of TNF-alpha in the control of endotoxin-induced acute-phase protein generation.


2004 ◽  
Vol 99 (3-4) ◽  
pp. 229-236 ◽  
Author(s):  
Fabrizio Ceciliani ◽  
Claudia Grossi ◽  
Alessia Giordano ◽  
Vanessa Pocacqua ◽  
Saverio Paltrinieri

Immunobiology ◽  
2019 ◽  
Vol 224 (5) ◽  
pp. 672-680 ◽  
Author(s):  
Mosale Seetharam Sumanth ◽  
Kandahalli Venkataranganayaka Abhilasha ◽  
Shancy Petsel Jacob ◽  
Vyala Hanumanthareddy Chaithra ◽  
Venkatesha Basrur ◽  
...  

2019 ◽  
Vol 235 ◽  
pp. 93-100 ◽  
Author(s):  
Gabriele Meroni ◽  
Valentina Zamarian ◽  
Cristina Prussiani ◽  
Valerio Bronzo ◽  
Cristina Lecchi ◽  
...  

2003 ◽  
Vol 14 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Tino Hochepied ◽  
Franklin G Berger ◽  
Heinz Baumann ◽  
Claude Libert

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hiroshi Watanabe ◽  
Rui Fujimura ◽  
Yuto Hiramoto ◽  
Ryota Murata ◽  
Kento Nishida ◽  
...  

AbstractThe molecular mechanism for acute kidney injury (AKI) and its progression to chronic kidney disease (CKD) continues to be unclear. In this study, we investigated the pathophysiological role of the acute phase protein α1-acid glycoprotein (AGP) in AKI and its progression to CKD using AGP KO mice. Plasma AGP levels in WT mice were increased by about 3.5-fold on day 1–2 after renal ischemia–reperfusion (IR), and these values then gradually decreased to the level before renal IR on day 7–14. On day 1 after renal IR, the AGP KO showed higher renal dysfunction, tubular injury and renal inflammation as compared with WT. On day 14, renal function, tubular injury and renal inflammation in WT had recovered, but the recovery was delayed, and renal fibrosis continued to progress in AGP KO. These results obtained from AGP KO were rescued by the administration of human-derived AGP (hAGP) simultaneously with renal IR. In vitro experiments using RAW264.7 cells showed hAGP treatment suppressed the LPS-induced macrophage inflammatory response. These data suggest that endogenously induced AGP in early renal IR functions as a renoprotective molecule via its anti-inflammatory action. Thus, AGP represents a potential target molecule for therapeutic development in AKI and its progression CKD.


2021 ◽  
Vol 104 (1) ◽  
pp. 806-817
Author(s):  
W.E. Brown ◽  
M. Garcia ◽  
L.K. Mamedova ◽  
K.R. Christman ◽  
M.G. Zenobi ◽  
...  

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