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Serum amyloid A, the major vertebrate acute-phase reactant Uhlar CM; Whitehead ASEur J Biochem 1999[Oct]; 265 (2): 501-23The serum amyloid A (SAA) family comprises a number of differentially expressed apolipoproteins, acute-phase SAAs (A-SAAs) and constitutive SAAs (C-SAAs). A-SAAs are major acute-phase reactants, the in vivo concentrations of which increase by as much as 1000-fold during inflammation. A-SAA mRNAs or proteins have been identified in all vertebrates investigated to date and are highly conserved. In contrast, C-SAAs are induced minimally, if at all, during the acute-phase response and have only been found in human and mouse. Although the liver is the primary site of synthesis of both A-SAA and C-SAA, extrahepatic production has been reported for most family members in most of the mammalian species studied. In vitro, the dramatic induction of A-SAA mRNA in response to pro-inflammatory stimuli is due largely to the synergistic effects of cytokine signaling pathways, principally those of the interleukin-1 and interleukin-6 type cytokines. This induction can be enhanced by glucocorticoids. Studies of the A-SAA promoters in several mammalian species have identified a range of transcription factors that are variously involved in defining both cytokine responsiveness and cell specificity. These include NF-kappaB, C/EBP, YY1, AP-2, SAF and Sp1. A-SAA is also post-transcriptionally regulated. Although the precise role of A-SAA in host defense during inflammation has not been defined, many potential clinically important functions have been proposed for individual SAA family members. These include involvement in lipid metabolism/transport, induction of extracellular-matrix-degrading enzymes, and chemotactic recruitment of inflammatory cells to sites of inflammation. A-SAA is potentially involved in the pathogenesis of several chronic inflammatory diseases: it is the precursor of the amyloid A protein deposited in amyloid A amyloidosis, and it has also been implicated in the pathogenesis of atheroscelerosis and rheumatoid arthritis.|Acute-Phase Proteins/genetics/*immunology[MESH]|Amyloidosis/etiology[MESH]|Animals[MESH]|Apolipoproteins/genetics/*immunology[MESH]|Arteriosclerosis/etiology[MESH]|Arthritis, Rheumatoid/etiology[MESH]|Cytokines/immunology[MESH]|Gene Expression Regulation/immunology[MESH]|Glucocorticoids/pharmacology[MESH]|Humans[MESH]|Inflammation/immunology[MESH]|Serum Amyloid A Protein/genetics/*immunology[MESH]|Signal Transduction/immunology[MESH]|Transcription, Genetic[MESH] |
