Serum amyloid A3 is pro-atherogenic

Joel C. Thompson, Patricia G. Wilson, Preetha Shridas, Ailing Ji, Maria de Beer, Frederick C. de Beer, Nancy R. Webb, Lisa R. Tannock

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


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.

Original languageEnglish
Pages (from-to)32-35
Number of pages4
StatePublished - Jan 2018

Bibliographical note

Funding Information:
This work was supported by funding from the Department of Veterans Affairs CX000622 (to LRT) and R01 HL134731 (to NRW, FCdB). There are no disclosures for any author.

Publisher Copyright:
© 2017


  • Atherosclerosis
  • Inflammation
  • Murine models

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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