| First Author | Ham D | Year | 1997 |
| Journal | Scand J Immunol | Volume | 45 |
| Issue | 4 | Pages | 354-60 |
| PubMed ID | 9105421 | Mgi Jnum | J:40098 |
| Mgi Id | MGI:87436 | Doi | 10.1046/j.1365-3083.1997.d01-408.x |
| Citation | Ham D, et al. (1997) Degradation of amyloid A precursor protein SAA by macrophage cell lines obtained from amyloid resistant and susceptible strains of mice. Scand J Immunol 45(4):354-60 |
| abstractText | Reactive AA amyloidosis can be induced in mice in a model of sustained inflammation following daily casein subcutaneous injections. However, the development of AA amyloidosis is known to vary in different strains of mice. The C57BL/6 strain is susceptible to the development of amyloidosis while the A/J strain is resistant. The degradation of purified serum amyloid A (SAA) protein by human monocytes as well as by mouse macrophages has been shown. The resistance/susceptibility of different mouse strains to the development of systemic amyloidosis may therefore be related to a difference in the ability of macrophages to degrade SAA. The authors have used bone marrow-derived macrophage cell lines obtained from susceptible C57BL/6 (ANA-1) and resistant A/J (A/J 10) mouse strains to compare their ability to degrade HDL-SAA in vitro. Cells were incubated with HDL-SAA for up to 72 h and the culture medium was analysed by SDS-PAGE to determine the rate of SAA degradation by the macrophages. The A/J 10 cells (resistant) were found to initiate a constant HDL-SAA degradation promptly whereas ANA-1 cells (susceptible) showed an intermittent block in the degradation of the precursor. Activation of macrophages by lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma) hampered the precursor degradation suggesting that the activation process may favour extracellular accumulation of the precursor leading to a partial degradation and fibril formation. |
