| First Author | Tannock LR | Year | 2018 |
| Journal | J Lipid Res | Volume | 59 |
| Issue | 2 | Pages | 339-347 |
| PubMed ID | 29247043 | Mgi Jnum | J:257498 |
| Mgi Id | MGI:6115118 | Doi | 10.1194/jlr.M080887 |
| Citation | Tannock LR, et al. (2018) Serum amyloid A3 is a high density lipoprotein-associated acute-phase protein. J Lipid Res 59(2):339-347 |
| abstractText | Serum amyloid A (SAA) is a family of acute-phase reactants. Plasma levels of human SAA1/SAA2 (mouse SAA1.1/2.1) can increase >/=1,000-fold during an acute-phase response. Mice, but not humans, express a third relatively understudied SAA isoform, SAA3. We investigated whether mouse SAA3 is an HDL-associated acute-phase SAA. Quantitative RT-PCR with isoform-specific primers indicated that SAA3 and SAA1.1/2.1 are induced similarly in livers ( approximately 2,500-fold vs. approximately 6,000-fold, respectively) and fat ( approximately 400-fold vs. approximately 100-fold, respectively) of lipopolysaccharide (LPS)-injected mice. In situ hybridization demonstrated that all three SAAs are produced by hepatocytes. All three SAA isoforms were detected in plasma of LPS-injected mice, although SAA3 levels were approximately 20% of SAA1.1/2.1 levels. Fast protein LC analyses indicated that virtually all of SAA1.1/2.1 eluted with HDL, whereas approximately 15% of SAA3 was lipid poor/free. After density gradient ultracentrifugation, isoelectric focusing demonstrated that approximately 100% of plasma SAA1.1 was recovered in HDL compared with only approximately 50% of SAA2.1 and approximately 10% of SAA3. Thus, SAA3 appears to be more loosely associated with HDL, resulting in lipid-poor/free SAA3. We conclude that SAA3 is a major hepatic acute-phase SAA in mice that may produce systemic effects during inflammation. |
