Publication: Extrahepatic production of acute phase serum amyloid A
Authors
Upragarin, N. ; Landman, W.J.M. ; Gaastra, W. ; Gruys, E.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Amyloidosis is a group of diseases
characterized by the extracellular deposition of protein
that contains non-branching, straight fibrils on electron
microscopy (amyloid fibrils) that have a high content of
ß-pleated sheet conformation. Various biochemically
distinct proteins can undergo transformation into
amyloid fibrils. The precursor protein of amyloid protein
A (AA) is the acute phase protein serum amyloid A
(SAA). The concentration of SAA in plasma increases
up to 1000-fold within 24 to 48 h after trauma,
inflammation or infection. Individuals with chronically
increased SAA levels may develop AA amyloidosis.
SAA has been divided into two groups according to the
encoding genes and the source of protein production.
These two groups are acute phase SAA (A-SAA) and
constitutive SAA (C-SAA). Although the liver is the
primary site of the synthesis of A-SAA and C-SAA,
extrahepatic production of both SAAs has been observed
in animal models and cell culture experiments of several
mammalian species and chicken. The functions of ASAA
are thought to involve lipid metabolism, lipid
transport, chemotaxis and regulation of the inflammatory
process. There is growing evidence that extrahepatic ASAA
formation may play a crucial role in
amyloidogenesis and enhances amyloid formation at the
site of SAA production.
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