Joel C Thompson1, Patricia G Wilson1, Preetha Shridas2, Ailing Ji1, Maria de Beer3, Frederick C de Beer2, Nancy R Webb4, Lisa R Tannock5. 1. Department of Veterans Affairs, Lexington, KY 40502, USA; Department of Internal Medicine, University of Kentucky, Lexington, KY, 40536, USA; Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, 40536, USA. 2. Department of Internal Medicine, University of Kentucky, Lexington, KY, 40536, USA; Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, 40536, USA. 3. Department of Physiology, University of Kentucky, Lexington, KY, 40536, USA; Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, 40536, USA. 4. Department of Veterans Affairs, Lexington, KY 40502, USA; Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, 40536, USA; Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, 40536, USA. 5. Department of Veterans Affairs, Lexington, KY 40502, USA; Department of Internal Medicine, University of Kentucky, Lexington, KY, 40536, USA; Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, 40536, USA. Electronic address: lisa.tannock@uky.edu.
Abstract
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. Published by Elsevier B.V.
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. Published by Elsevier B.V.
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