@article{oai:soar-ir.repo.nii.ac.jp:00021777,
 author = {Yang, Mu and Liu, Yingye and Dai, Jian and Li, Lin and Ding, Xin and Xu, Zhe and Mori, Masayuki and Miyahara, Hiroki and Sawashita, Jinko and Higuchi, Keiichi},
 journal = {SCIENTIFIC REPORTS},
 month = {Apr},
 note = {During acute-phase response (APR), there is a dramatic increase in serum amyloid A (SAA) in plasma high density lipoproteins (HDL). Elevated SAA leads to reactive AA amyloidosis in animals and humans. Herein, we employed apolipoprotein A-II (ApoA-II) deficient (Apoa2(-/-)) and transgenic (Apoa2Tg) mice to investigate the potential roles of ApoA-II in lipoprotein particle formation and progression of AA amyloidosis during APR. AA amyloid deposition was suppressed in Apoa2(-/-) mice compared with wild type (WT) mice. During APR, Apoa2(-/-) mice exhibited significant suppression of serum SAA levels and hepatic Saa1 and Saa2 mRNA levels. Pathological investigation showed Apoa2(-/-) mice had less tissue damage and less inflammatory cell infiltration during APR. Total lipoproteins were markedly decreased in Apoa2(-/-) mice, while the ratio of HDL to low density lipoprotein (LDL) was also decreased. Both WT and Apoa2(-/-) mice showed increases in LDL and very large HDL during APR. SAA was distributed more widely in lipoprotein particles ranging from chylomicrons to very small HDL in Apoa2(-/-) mice. Our observations uncovered the critical roles of ApoA-II in inflammation, serum lipoprotein stability and AA amyloidosis morbidity, and prompt consideration of therapies for AA and other amyloidoses, whose precursor proteins are associated with circulating HDL particles., Article, SCIENTIFIC REPORTS.8:5620(2018)},
 title = {Apolipoprotein A-II induces acute-phase response associated AA amyloidosis in mice through conformational changes of plasma lipoprotein structure},
 volume = {8},
 year = {2018}
}