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Changes in Plasma Apolipoprotein AI and AII Concentrations in Murine Reactive Amyloidosis
Author(s) -
Toshiyuki Yamada,
Atsufumi Wada,
Takeaki Fukuda,
Yoshio Itoh,
Kouichi Itoh
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00621.x
Subject(s) - amyloidosis , apolipoprotein b , plasma lipoprotein , medicine , endocrinology , chemistry , cholesterol , lipoprotein
Based on the recent findings that patients with systemic amyloidosis have reduced plasma apolipoprotein AII (apoAII) concentrations, this study assessed the behaviour of apolipoprotein AI (apoAI) and apoAII in a murine model of reactive amyloidosis. ICR mice were subjected to a single inflammatory stimulus and then sacrificed at the end of week 1 (group I), week 2 (group II) or week 8 (group III). Amyloid deposits were found in approximately one‐half of the animals. Plasma apoAI and apoAII concentrations were reduced in all stimulated animals compared with control animals. In groups II and III, apoAII and apoAII/apoAI ratios were lower in the amyloidotic animals than in nonamyloidotic animals, similar to findings in the human amyloidosis patients. Both apoAI and apoAII mRNA in the liver were reduced in group I, but not in group II or III. Both apoAI and apoAII were detected immunohistochemically in the amyloid deposits in groups I and II, but not in group III. Thus, the reduction of plasma apoAs in the amyloid‐forming phase may be due, in part, to the involvement of high‐density lipoproteins in the deposits. However, that in the chronic phase may be affected by other mechanisms.