| First Author | Thompson JC | Year | 2018 |
| Journal | Atherosclerosis | Volume | 268 |
| Pages | 32-35 | PubMed ID | 29175652 |
| Mgi Jnum | J:280231 | Mgi Id | MGI:6369117 |
| Doi | 10.1016/j.atherosclerosis.2017.11.011 | Citation | Thompson JC, et al. (2018) Serum amyloid A3 is pro-atherogenic. Atherosclerosis 268:32-35 |
| abstractText | BACKGROUND AND AIMS: Serum amyloid A (SAA) predicts cardiovascular events. Overexpression of SAA increases atherosclerosis development; however, deficiency of two of the murine acute phase isoforms, SAA1.1 and SAA2.1, has no effect on atherosclerosis. SAA3 is a pseudogene in humans, but is an expressed acute phase isoform in mice. The goal of this study was to determine if SAA3 affects atherosclerosis in mice. METHODS: ApoE(-/-) mice were used as the model for all studies. SAA3 was overexpressed by an adeno-associated virus or suppressed using an anti-sense oligonucleotide approach. RESULTS: Over-expression of SAA3 led to a 4-fold increase in atherosclerosis lesion area compared to control mice (p = 0.01). Suppression of SAA3 decreased atherosclerosis in mice genetically deficient in SAA1.1 and SAA2.1 (p < 0.0001). CONCLUSIONS: SAA3 augments atherosclerosis in mice. Our results resolve a previous paradox in the literature and support extensive epidemiological data that SAA is pro-atherogenic. |
