Diverse gene expression for isotypes of murine serum amyloid A protein during acute phase reaction

Science ◽  
1986 ◽  
Vol 232 (4747) ◽  
pp. 227-229 ◽  
Author(s):  
K Yamamoto ◽  
M Shiroo ◽  
S Migita
2009 ◽  
Vol 296 (6) ◽  
pp. F1355-F1363 ◽  
Author(s):  
Katherine J. Kelly ◽  
Barbara Kluve-Beckerman ◽  
Jesus H. Dominguez

Serum amyloid A protein (SAA) surges 1,000-fold in the blood of acute-phase animals, and yet its function during these acute events remains unknown. We report herein that SAA stimulates a developmental program in cultured NRK-52E cells that culminates in differentiated and functional tubules that feature a proximal tubule phenotype. We also found strong SAA expression in states of tubule formation (in utero stage) and regeneration (recovery from ischemia-reperfusion injury). These data lend support to a novel view of a more localized renal acute-phase reaction, where renal SAA may act as a paracrine or autocrine molecule that promotes tubule formation during development and repair.


2020 ◽  
pp. 2199-2207
Author(s):  
Mark B. Pepys

The acute phase response—trauma, tissue necrosis, infection, inflammation, and malignant neoplasia induce a complex series of nonspecific systemic, physiological, and metabolic responses including fever, leucocytosis, catabolism of muscle proteins, greatly increased de novo synthesis and secretion of a number of ‘acute phase’ plasma proteins, and decreased synthesis of albumin, transthyretin, and high- and low-density lipoproteins. The altered plasma protein concentration profile is called the acute phase response. Acute phase proteins—these are mostly synthesized by hepatocytes, in which transcription is controlled by cytokines including interleukin 1, interleukin 6, and tumour necrosis factor. The circulating concentrations of complement proteins and clotting factors increase by up to 50 to 100%; some of the proteinase inhibitors and α‎1-acid glycoprotein can increase three- to fivefold; but C-reactive protein (CRP) and serum amyloid A protein (an apolipoprotein of high-density lipoprotein particles) are unique in that their concentrations can change by more than 1000-fold. C-reactive protein—this consists of five identical, nonglycosylated, noncovalently associated polypeptide subunits. It binds to autologous and extrinsic materials which contain phosphocholine, including bacteria and their products. Ligand-bound CRP activates the classical complement pathway and triggers the inflammatory and opsonizing activities of the complement system, thereby contributing to innate host resistance to pneumococci and probably to recognition and safe ‘scavenging’ of cellular debris. Clinical features—(1) determination of CRP in serum or plasma is the most useful marker of the acute phase response in most inflammatory and tissue damaging conditions. (2) Acute phase proteins may be harmful in some circumstances. Sustained increased production of serum amyloid A protein can lead to the deposition of AA-type, reactive systemic amyloid.


1988 ◽  
Vol 255 (1) ◽  
pp. 29-34 ◽  
Author(s):  
A E Nel ◽  
M C De Beer ◽  
E G Shephard ◽  
A F Strachan ◽  
M L Vandenplas ◽  
...  

Monokine-induced hepatic secretion of serum amyloid A protein (apo-SAA), an acute-phase reactant, is followed by rapid association with high-density lipoprotein (HDL) in plasma. Plasma clearance of apo-SAA is more rapid than any of the other HDL apolipoproteins. It has been shown that, of the acute-phase HDL3 apolipoproteins, apo-SAA preferentially associates with neutrophil membranes. HDL apolipoproteins have been shown to activate protein kinase C in endothelial cells. We therefore investigated potential phosphorylation of HDL3 apolipoproteins by protein kinase C. Apo-SAA was the only apolipoprotein phosphorylated (Km = 12 mM). Phosphorylation of the apo-SAA-containing HDL3 particle was selective for the more basic isoforms of apo-SAA (pI 7.0, 7.4, 7.5 and 8.0), with more acidic isoforms being phosphorylated when delipidated acute-phase apolipoproteins were used as substrate. However, phosphorylation was not in itself responsible for the establishment of the apo-SAA isoforms.


Author(s):  
Martin-Tino Časl ◽  
Mirjana Sabljar-Matovinović ◽  
Sandra Kovačević ◽  
Darko Počanić ◽  
Vladimira Preden-Kereković ◽  
...  

We have evaluated the clinical relevance of monitoring acute phase proteins in severe urinary tract infection. Body temperature, white blood cell count, erythrocyte sedimentation rate, serum amyloid A protein (SAA), C-reactive protein (CRP), α-1-antichymotrypsin (ACT) and α-1-acid glycoprotein (AGP) were determined daily in sera from 18 treated patients. Two patterns of response could be identified: responders and non-responders whose therapy had to be changed. Mean values for each acute phase protein were calculated daily in both responders and non-responders. Statistical evaluation of the significance between the means for each protein was also performed on a daily basis and showed P < 0·01 for SAA and CRP on day 3, for ACT on day 5, and for AGP on day 6. SAA and CRP appear to be the most reliable markers for antimicrobial therapy monitoring in patients with urinary tract infections.


1993 ◽  
Vol 37 (4) ◽  
pp. 447-451 ◽  
Author(s):  
P. V. SYVERSEN ◽  
J. JUUL ◽  
M. RYGG ◽  
K. SLETTEN ◽  
G. HUSBY ◽  
...  

1998 ◽  
Vol 334 (3) ◽  
pp. 489-503 ◽  
Author(s):  
Liselotte E. JENSEN ◽  
Alexander S. WHITEHEAD

The acute-phase (AP) serum amyloid A proteins (A-SAA) are multifunctional apolipoproteins which are involved in cholesterol transport and metabolism, and in modulating numerous immunological responses during inflammation and the AP response to infection, trauma or stress. During the AP response the hepatic biosynthesis of A-SAA is up-regulated by pro-inflammatory cytokines, and circulating concentrations can increase by up to 1000-fold. Chronically elevated A-SAA concentrations are a prerequisite for the pathogenesis of secondary amyloidosis, a progressive and fatal disease characterized by the deposition in major organs of insoluble plaques composed principally of proteolytically cleaved A-SAA, and may also contribute to physiological processes that lead to atherosclerosis. There is therefore a requirement for both positive and negative control mechanisms that permit the rapid induction of A-SAA expression until it has fulfilled its host-protective function(s) and subsequently ensure that its expression can be rapidly returned to baseline. These mechanisms include modulation of promoter activity involving, for example, the inducer nuclear factor κB (NF-κB) and its inhibitor IκB, up-regulatory transcription factors of the nuclear factor for interleukin-6 (NF-IL6) family and transcriptional repressors such as yin and yang 1 (YY1). Post-transcriptional modulation involving changes in mRNA stability and translation efficiency permit further up- and down-regulatory control of A-SAA protein synthesis to be achieved. In the later stages of the AP response, A-SAA expression is effectively down-regulated via the increased production of cytokine antagonists such as the interleukin-1 receptor antagonist (IL-1Ra) and of soluble cytokine receptors, resulting in less signal transduction driven by pro-inflammatory cytokines.


Genomics ◽  
1993 ◽  
Vol 16 (2) ◽  
pp. 447-454 ◽  
Author(s):  
Diana M. Steel ◽  
Grant C. Sellar ◽  
Clarissa M. Uhlar ◽  
Susan Simon ◽  
Fred C. DeBeer ◽  
...  

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