Abstract
Serum amyloid A protein (apo SAA) is an acute phase protein associated with high density lipoprotein (HDL) in serum. SAA is the precursor of tissue amyloid A, which deposits as amyloid fibrils in secondary amyloidosis.
We obtained the specific polyclonal antibody against human apo SAA. Using immunoblotting and histochemical methods with this antibody, the following results were observed.
1) Apo SAA was detected in HDL fraction of the plasma from patients with acute myocardial infarction by immunoblotting on two-dimensional electrophoresis. Studies of four patients with acute myocardial infarction revealed that the quantity of apo SAA in the HDL3 fraction was about 3.5 times larger than that in HDL2. Apo SAA accounted for 18.5±3.1% (mean±SD) of the concentration of HDL3 constituents in the patients. Moreover, each relative proportion of apo A-I, A-II and phospholipid in apo SAA-containing HDL3 was decreased as compared with normal HDL3 (27.1±1.7% vs. 36.0±2.5%, 5.3±0.6 vs. 8.7+1.0, 25.5±3.2 vs. 32.9±0.9, respectively). These results suggest that apo SAA displaces some of the apo A-I, apo A-II and phospholipid which exist in the surface shell of the HDL particle. Furthermore, the particle size of apo SAA containing-HDL3 (mean radius 5.46±0.12nm) was larger than that of normal HDL3 (5.22±0.03nm) as measured by gradient gel electrophoresis. We thought that apo SAA containing-HDL was remodeled based on its particle composition, and in consequence the function of HDL including reverse cholesterol transfer system might be affected.
2) Apo SAA was detected in the intima of the atherosclerotic lesion of the human coronary artery and abdominal aorta by immunohistochemical method, and the localization was quite similar to that of apo B. Apo SAA was also detected in the extract from the atherosclerotic lesion of the abdominal aorta by homogenization with 10% formic acid. These results suggest that apo SAA may be involved directly in the process of atherogenesis.
We conclude that apo SAA containing-HDL might play a role in the pathogenesis of atherosclerosis.
