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

doi:10.1016/j.atherosclerosis.2017.11.011

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 journal › Article › peer-review

52 Scopus citations

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.

Original language	English
Pages (from-to)	32-35
Number of pages	4
Journal	Atherosclerosis
Volume	268
DOIs	https://doi.org/10.1016/j.atherosclerosis.2017.11.011
State	Published - Jan 2018

Bibliographical note

Publisher Copyright:
© 2017

Funding

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.

Funders	Funder number
National Institute of General Medical Sciences	P20GM103527
U.S. Department of Veterans Affairs	R01 HL134731, CX000622

Keywords

Atherosclerosis
Inflammation
Murine models

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/j.atherosclerosis.2017.11.011

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title = "Serum amyloid A3 is pro-atherogenic",

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.",

keywords = "Atherosclerosis, Inflammation, Murine models",

author = "Thompson, {Joel C.} and Wilson, {Patricia G.} and Preetha Shridas and Ailing Ji and {de Beer}, Maria and {de Beer}, {Frederick C.} and Webb, {Nancy R.} and Tannock, {Lisa R.}",

note = "Publisher Copyright: {\textcopyright} 2017",

year = "2018",

month = jan,

doi = "10.1016/j.atherosclerosis.2017.11.011",

language = "English",

volume = "268",

pages = "32--35",

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AU - Thompson, Joel C.

AU - Wilson, Patricia G.

AU - Shridas, Preetha

AU - Ji, Ailing

AU - de Beer, Maria

AU - de Beer, Frederick C.

AU - Webb, Nancy R.

AU - Tannock, Lisa R.

PY - 2018/1

Y1 - 2018/1

N2 - 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.

AB - 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.

KW - Atherosclerosis

KW - Inflammation

KW - Murine models

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ER -

Serum amyloid A3 is pro-atherogenic

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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