Serum Amyloid A Human ELISA Kit

Several isoforms of serum amyloid A (SAA) have been identified so far and because the plasma concentration of it increases dramatically, it is used as an indicator of inflammation in animals. In many terrestrial mammals, the circulating isoforms are SAA1 and SAA2, which are synthesized in the liver. Extra-hepatically synthesized SAA3, however, is a predominantly local SAA isoform with a characteristic N-terminal TFLK motif and a highly alkaline isoelectric point (pI). The aim of this study was to characterize the circulating SAA isoforms in bottlenose dolphins (dSAA) by determining the deduced amino acid sequence isolated from liver and the pI of plasma from healthy dolphins and those with inflammation. The deduced amino acid sequences of dSAA showed characteristics of SAA3 with an N-terminal TFLK motif, a predicted alkaline pI and were phylogenetically clustered with the SAA3 group rather than the SAA1 and SAA2 groups. Various tissues contained dSAA mRNA with the highest levels being detected in the liver. Isoelectric focusing and western blot analysis showed that one highly alkaline SAA was markedly detected in plasma obtained from dolphins affected by inflammation. These results suggest that, unlike other mammals, the circulating SAA in dolphins exhibits SAA3 properties, as is the case in pigs. (C) 2012 Elsevier B.V. All rights reserved.

Purpose of reviewAtherosclerosis is a chronic inflammation associated with increased expression of the acute phase isoforms of serum amyloid A (SAA) and in humans is a plasma biomarker for future cardiovascular events. However, whether SAA is only a biomarker or participates in the development of cardiovascular disease is not well characterized. The purpose of this review is to summarize putative functions of SAA relevant to atherogenesis and in-vivo murine studies that directly examine the effect of SAA on atherosclerosis.Recent findingsModulation of the expression of SAA1 and/or SAA2 in murine models of atherosclerosis suggests that SAA promotes early atherogenesis. SAA secreted from bone-marrow-derived cells contributes to this antiatherogenic phenotype. SAA also promotes angiotensin-induced abdominal aneurysm in atherogenic mouse models. The reduction in atherosclerosis may be due, at least in part, to remodeling of the acute phase HDL to reduce its capacity to promote cholesterol efflux and reduce its anti-inflammatory ability.SummarySAA is more than a marker of cardiovascular disease and is a participant in the early atherogenic process.