Regulation of the acute phase response genes alpha1-acid glycoprotein and alpha1-antitrypsin correlates with sensitivity to thermal injury

Exposing rats to a single session of inescapable tail shock (IS) reduces corticosteroid binding globulin (CBG) 24 h later (Fleshner et al., Endocrinology 136: 5336–5342, 1995). The present experiments examined whether reductions in CBG are differentially affected by controllable vs. identical uncontrollable tail shock, are mediated by IS-induced glucocorticoid elevation, or reflect IS-induced activation of the acute phase response and whether IS produces fever. The results demonstrate that 1) equivalent reductions in CBG are observed in response to escapable tail shock or yoked IS, 2) IS-induced CBG reduction is not blocked by adrenalectomy in rats that receive basal corticosteroid replacement or by pretreatment with RU-38486, and 3) IS appears to activate the acute phase response, since IS reduces serum levels of an acute-phase negative reactant (CBG), increases serum levels of acute-phase positive reactants (haptoglobin and α1-acid glycoprotein), and increases core body temperature 20–24 h later.

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Expression of the α1-acid glycoprotein gene in fetal rat liver during acute phase response

Comparative Biochemistry and Physiology Part A Molecular & Integrative Physiology ◽

10.1016/s1095-6433(99)90456-7 ◽

1999 ◽

Vol 124 ◽

pp. S115

Author(s):

M Mihailovic ◽

M Petrovic ◽

Z Milicevic ◽

D Bogojevic

Keyword(s):

Rat Liver ◽

Acute Phase ◽

Acute Phase Response ◽

Phase Response ◽

Acid Glycoprotein ◽

Glycoprotein Gene ◽

Fetal Rat ◽

Fetal Rat Liver

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In vitro release of ?1-acid glycoprotein RNA sequences shows fidelity with the acute phase response in vivo

Molecular Biology Reports ◽

10.1007/bf00419737 ◽

1986 ◽

Vol 11 (3) ◽

pp. 163-172 ◽

Cited By ~ 7

Author(s):

G. A. Clawson ◽

J. Button ◽

C. H. Woo ◽

Yu-Cheng Liao ◽

E. A. Smuckler

Keyword(s):

Acute Phase ◽

Acute Phase Response ◽

In Vitro Release ◽

Phase Response ◽

Rna Sequences ◽

Acid Glycoprotein ◽

Vitro Release

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Evidence for a novel, local acute-phase response in the bovine oviduct: Progesterone and lipopolysaccharide up-regulate alpha 1-acid-glycoprotein expression in epithelial cells in vitro

Molecular Reproduction and Development ◽

10.1002/mrd.22355 ◽

2014 ◽

Vol 81 (9) ◽

pp. 861-870 ◽

Cited By ~ 17

Author(s):

R. Kowsar ◽

N. Hambruch ◽

M.A. Marey ◽

J. Liu ◽

T. Shimizu ◽

...

Keyword(s):

Epithelial Cells ◽

Acute Phase ◽

Acute Phase Response ◽

Phase Response ◽

Acid Glycoprotein

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The Hepatic Acute Phase Response to Thermal Injury

Acute Phase Proteins - Regulation and Functions of Acute Phase Proteins ◽

10.5772/18591 ◽

2011 ◽

Author(s):

Marc G.

Keyword(s):

Acute Phase ◽

Acute Phase Response ◽

Thermal Injury ◽

Phase Response

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Studies on monokines as mediators of the acute phase response: Effects on sialyltransferase, albumin, α1-acid glycoprotein and β-N-acetylhexosaminidase

Biochemical and Biophysical Research Communications ◽

10.1016/0006-291x(85)90377-8 ◽

1985 ◽

Vol 130 (1) ◽

pp. 30-36 ◽

Cited By ~ 25

Author(s):

B.M.R.N.J. Woloski ◽

E. Gospodarek ◽

J.C. Jamieson

Keyword(s):

Acute Phase ◽

Acute Phase Response ◽

Phase Response ◽

Acid Glycoprotein

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Glycoprotein biosynthesis during the acute-phase response to inflammation

Canadian Journal of Biochemistry and Cell Biology ◽

10.1139/o83-133 ◽

1983 ◽

Vol 61 (9) ◽

pp. 1041-1048 ◽

Cited By ~ 36

Author(s):

J. C. Jamieson ◽

H. A. Kaplan ◽

B. M. R. N. J. Woloski ◽

M. Hellman ◽

K. Ham

Keyword(s):

Acute Phase ◽

Acute Phase Response ◽

Elevated Serum ◽

Serum Cortisol ◽

Serum Levels ◽

Acute Phase Reactant ◽

Phase Response ◽

Acute Phase Reactants ◽

Acid Glycoprotein ◽

Phase Reactant

Inflammation results in an increase in the levels of a variety of glycoproteins in serum. The glycoproteins that respond in this way are usually referred to as acute-phase reactants. Studies on the acute-phase response of rat α1-acid glycoprotein showed that there was an increase in the liver levels of this glycoprotein at 12 h after turpentine inflammation. This was followed by increased serum levels at 48–72 h after inflammation, suggesting a precursor–product relationship between liver and serum α1-acid glycoprotein. Incorporation studies coupled with measurements of synthesis rates of α1-acid glycoprotein showed that increased synthesis was responsible for the acute-phase response of this protein to inflammation. These studies also showed that albumin was a negative acute-phase reactant. The acute-phase response of α1-acid glycoprotein was accompanied by increased liver pools of UDP–N-acetylglucosamine (UDP–GlcNAc) and UDP–N-acetylgalactosamine (UDP–GalNAc) and increased liver activities of glucosamine-6-phosphate synthase and UDP–GlcNAc 2-epimerase. Activities of galactosyl and sialyl transferases in liver were also elevated and serum sialyl transferase was increased substantially in inflammation, suggesting that it may also be an acute-phase reactant. Liver activities of β-N-acetylhexosaminidase and β-galactosidase declined by about 50% at 24 h after inflammation; there was evidence that serum levels of these enzymes increased at 24–72 h after inflammation, suggesting that the lysosomal glycosidases may be released from liver during inflammation. Inflammation resulted in elevated serum Cortisol, insulin, and adrenocorticotropic hormone and induced increased glycogenosis; liver cAMP levels were also increased during inflammation. Preliminary studies are presented to show that leukocyte-derived factors may be involved in the acute-phase response of α1-acid glycoprotein to inflammation.

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