scholarly journals Serum Amyloid A and High Density Lipoprotein Participate in the Acute Phase Response of Kawasaki Disease

1997 ◽  
Vol 42 (5) ◽  
pp. 651-655 ◽  
Author(s):  
Veneracion G Cabana ◽  
Samuel S Gidding ◽  
Godfrey S Getz ◽  
Jennifer Chapman ◽  
Stanford T Shulman
Keyword(s):  
Kawasaki Disease ◽  
High Density Lipoprotein ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Amyloid A ◽  
Density Lipoprotein ◽  
High Density ◽  
Phase Response ◽  
Serum Amyloid ◽  
Amyloid A

Serum amyloid A and high density lipoproteins during the acute phase response

1988 ◽  
Vol 18 (6) ◽  
pp. 619-626 ◽  
Author(s):  
LINDA L. BAUSSERMAN ◽  
D. N. BERNIER ◽  
K. P. W. J. McADAM ◽  
P. N. HERBERT
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Amyloid A ◽  
High Density ◽  
Phase Response ◽  
Serum Amyloid ◽  
High Density Lipoproteins ◽  
Amyloid A

scholarly journals Heparan Sulfate Dissociates Serum Amyloid A (SAA) from Acute-phase High-density Lipoprotein, Promoting SAA Aggregation

2012 ◽  
Vol 287 (30) ◽  
pp. 25669-25677 ◽  
Author(s):  
Fredrik Noborn ◽  
John B. Ancsin ◽  
Wimal Ubhayasekera ◽  
Robert Kisilevsky ◽  
Jin-Ping Li
Keyword(s):  
High Density Lipoprotein ◽  
Heparan Sulfate ◽  
Acute Phase ◽  
Serum Amyloid A ◽  
Density Lipoprotein ◽  
High Density ◽  
Serum Amyloid ◽  
Amyloid A

scholarly journals The role of serum amyloid A and sphingosine-1-phosphate on high-density lipoprotein functionality

2015 ◽  
Vol 396 (6-7) ◽  
pp. 573-583 ◽  
Author(s):  
Nicole Prüfer ◽  
Burkhard Kleuser ◽  
Markus van der Giet
Keyword(s):  
High Density Lipoprotein ◽  
Acute Phase ◽  
Serum Amyloid A ◽  
Biological Activities ◽  
Density Lipoprotein ◽  
High Density ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Hdl Function ◽  
Sphingosine 1 Phosphate

Abstract The high-density lipoprotein (HDL) is one of the most important endogenous cardiovascular protective markers. HDL is an attractive target in the search for new pharmaceutical therapies and in the prevention of cardiovascular events. Some of HDL’s anti-atherogenic properties are related to the signaling molecule sphingosine-1-phosphate (S1P), which plays an important role in vascular homeostasis. However, for different patient populations it seems more complicated. Significant changes in HDL’s protective potency are reduced under pathologic conditions and HDL might even serve as a proatherogenic particle. Under uremic conditions especially there is a change in the compounds associated with HDL. S1P is reduced and acute phase proteins such as serum amyloid A (SAA) are found to be elevated in HDL. The conversion of HDL in inflammation changes the functional properties of HDL. High amounts of SAA are associated with the occurrence of cardiovascular diseases such as atherosclerosis. SAA has potent pro-atherogenic properties, which may have impact on HDL’s biological functions, including cholesterol efflux capacity, antioxidative and anti-inflammatory activities. This review focuses on two molecules that affect the functionality of HDL. The balance between functional and dysfunctional HDL is disturbed after the loss of the protective sphingolipid molecule S1P and the accumulation of the acute-phase protein SAA. This review also summarizes the biological activities of lipid-free and lipid-bound SAA and its impact on HDL function.

scholarly journals Acute-phase high-density lipoprotein in the rat does not contain serum amyloid A protein

1987 ◽  
Vol 242 (1) ◽  
pp. 301-303 ◽  
Author(s):  
M L Baltz ◽  
I F Rowe ◽  
D Caspi ◽  
W G Turnell ◽  
M B Pepys
Keyword(s):  
High Density Lipoprotein ◽  
Acute Phase ◽  
Serum Amyloid A ◽  
Amyloid Fibrils ◽  
Density Lipoprotein ◽  
Lipid Binding ◽  
High Density ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Serum Amyloid A Protein

Serum amyloid A protein (SAA) is an acute-phase apolipoprotein of high-density lipoprotein (HDL). Its N-terminal sequence is identical with that of amyloid A protein (AA), the subunit of AA amyloid fibrils. However, rats do not develop AA amyloidosis, and we report here that neither normal nor acute-phase rat HDL contains a protein corresponding to SAA of other species. mRNA coding for a sequence homologous with the C-terminal but not with the N-terminal part of human SAA is synthesized in greatly increased amounts in acute-phase rat liver. These observations indicate that the failure of rats to develop AA amyloid results from the absence of most of the AA-like part of their SAA-like protein, and that the N-terminal portion of SAA probably contains the lipid-binding sequences.

scholarly journals Serum amyloid A-containing human high density lipoprotein 3. Density, size, and apolipoprotein composition.

1986 ◽  
Vol 261 (21) ◽  
pp. 9644-9651 ◽  
Author(s):  
G A Coetzee ◽  
A F Strachan ◽  
D R van der Westhuyzen ◽  
H C Hoppe ◽  
M S Jeenah ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Serum Amyloid A ◽  
Density Lipoprotein ◽  
High Density ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Human High Density Lipoprotein

The acute phase response and C-reactive protein

2020 ◽  
pp. 2199-2207
Author(s):  
Mark B. Pepys
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Amyloid A ◽  
Acute Phase Proteins ◽  
Phase Response ◽  
Serum Amyloid ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Amyloid A ◽  
Serum Amyloid A Protein

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.

Sign in / Sign up

Export Citation Format

Share Document