期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 400, 期 4, 页码 559-562出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.08.101
关键词
Amyloid; AA amyloidosis; Exosome; Amyloid-enhancing factor; Serum amyloid A
资金
- Amyloidosis Research Committee
- Ministry of Health and Welfare of Japan
- Charitable Trust Clinical Pathology Research Foundation of Japan
- Ministry of Education, Science, Sports and Culture of Japan [17390254, 21390270, 21790541]
- Grants-in-Aid for Scientific Research [21790541] Funding Source: KAKEN
Recent studies clearly demonstrated that several types of pathogenic amyloid proteins acted as agents that could transmit amyloidosis by means of a prion-like mechanism. Systemic AA amyloidosis is one of the most severe complications of chronic inflammatory disorders, particularly rheumatoid arthritis. It is well known that, similar to an infectious prion protein, amyloid-enhancing factor (AEF) acts as a transmissible agent in AA amyloidosis. However, how AEF transmits AA amyloidosis in vivo remained to be fully elucidated. In the present study, we focused on finding cell-free forms of AEF and its carriers in circulation by using the murine transfer model of AA amyloidosis. We first determined that circulating cell-free AEF existed in blood and plasma in mice with systemic AA amyloidosis. Second, we established that plasma exosomes containing AA amyloid oligomers derived from serum amyloid A had AEF activity and could transmit systemic AA amyloidosis via a prion-like mechanism. These novel findings should provide insights into the transmission mechanism of systemic amyloidoses. (C) 2010 Elsevier Inc. All rights reserved.
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