FOS expression in blood as a LDL-independent marker of statin treatment

Ju Gyeong Kang; Ho Joong Sung; Sarah I. Jawed; Cynthia L. Brenneman; Yesoda N. Rao; Salman Sher; Flavia M. Facio; Leslie G. Biesecker; Arshed A. Quyyumi; Vandana Sachdev; Paul M. Hwang

doi:10.1016/j.atherosclerosis.2010.06.023

FOS expression in blood as a LDL-independent marker of statin treatment

Ju Gyeong Kang, Ho Joong Sung, Sarah I. Jawed, Cynthia L. Brenneman, Yesoda N. Rao, Salman Sher, Flavia M. Facio, Leslie G. Biesecker, Arshed A. Quyyumi, Vandana Sachdev, Paul M. Hwang

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Objectives: The expression of FOS, a gene critical for monocyte and macrophage function, can be inhibited by statins through the disruption of a cholesterol-independent signaling pathway. In this pilot study, we hypothesized that blood FOS mRNA levels will be sensitive to statin treatment independent of LDL cholesterol levels. Methods: Three cohorts at increased risk of or with cardiovascular disease (CVD) were studied. Blood FOS mRNA levels were measured before and after statin treatment or in patients under stable treatment. Results: Statin treatment for three months significantly reduced blood FOS mRNA and LDL cholesterol levels. However, in subjects with similar LDL levels achieved by different doses of long term statin treatment, there was an inverse relationship between statin dose and FOS expression. Conclusions: FOS mRNA levels appear to be a sensitive marker of statin treatment that is dissociated from cholesterol levels.

Original language	English (US)
Pages (from-to)	567-570
Number of pages	4
Journal	Atherosclerosis
Volume	212
Issue number	2
DOIs	https://doi.org/10.1016/j.atherosclerosis.2010.06.023
State	Published - Oct 2010
Externally published	Yes

Keywords

Atherosclerosis
Biomarker
Blood
FOS
Gene expression
Inflammation
Macrophage
Monocyte
Pleiotropic
Statin

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/j.atherosclerosis.2010.06.023

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@article{2d1297061b404c97b62af2f13d44147f,

title = "FOS expression in blood as a LDL-independent marker of statin treatment",

abstract = "Objectives: The expression of FOS, a gene critical for monocyte and macrophage function, can be inhibited by statins through the disruption of a cholesterol-independent signaling pathway. In this pilot study, we hypothesized that blood FOS mRNA levels will be sensitive to statin treatment independent of LDL cholesterol levels. Methods: Three cohorts at increased risk of or with cardiovascular disease (CVD) were studied. Blood FOS mRNA levels were measured before and after statin treatment or in patients under stable treatment. Results: Statin treatment for three months significantly reduced blood FOS mRNA and LDL cholesterol levels. However, in subjects with similar LDL levels achieved by different doses of long term statin treatment, there was an inverse relationship between statin dose and FOS expression. Conclusions: FOS mRNA levels appear to be a sensitive marker of statin treatment that is dissociated from cholesterol levels.",

keywords = "Atherosclerosis, Biomarker, Blood, FOS, Gene expression, Inflammation, Macrophage, Monocyte, Pleiotropic, Statin",

author = "Kang, {Ju Gyeong} and Sung, {Ho Joong} and Jawed, {Sarah I.} and Brenneman, {Cynthia L.} and Rao, {Yesoda N.} and Salman Sher and Facio, {Flavia M.} and Biesecker, {Leslie G.} and Quyyumi, {Arshed A.} and Vandana Sachdev and Hwang, {Paul M.}",

note = "Funding Information: The authors wish to thank Drs. Ping-yuan Wang, Myron A. Waclawiw, Michael Sack and Toren Finkel for helpful discussions. We also thank Amy Linn, Danielle Singer, Paul Gobourne and Laurel Mendelsohn and Dr. George Csako for sample and data collection. This research was supported by the Intramural Research Program of the NHLBI and NHGRI, NIH, and the National Center for Research Resources (NCRR) Grant M01-RR00039 for the Emory General Clinical Research Center (GCRC). Funding Information: Dr. Quyyumi has received research funding from Pfizer, which manufactures atorvastatin, a product related to the research described in this paper and has received honoraria as a consultant. The terms of this arrangement have been reviewed and approved by Emory University in accordance with its conflict of interest policies. ",

year = "2010",

month = oct,

doi = "10.1016/j.atherosclerosis.2010.06.023",

language = "English (US)",

volume = "212",

pages = "567--570",

journal = "Atherosclerosis",

issn = "0021-9150",

publisher = "Elsevier Ireland Ltd",

number = "2",

}

TY - JOUR

T1 - FOS expression in blood as a LDL-independent marker of statin treatment

AU - Kang, Ju Gyeong

AU - Sung, Ho Joong

AU - Jawed, Sarah I.

AU - Brenneman, Cynthia L.

AU - Rao, Yesoda N.

AU - Sher, Salman

AU - Facio, Flavia M.

AU - Biesecker, Leslie G.

AU - Quyyumi, Arshed A.

AU - Sachdev, Vandana

AU - Hwang, Paul M.

N1 - Funding Information: The authors wish to thank Drs. Ping-yuan Wang, Myron A. Waclawiw, Michael Sack and Toren Finkel for helpful discussions. We also thank Amy Linn, Danielle Singer, Paul Gobourne and Laurel Mendelsohn and Dr. George Csako for sample and data collection. This research was supported by the Intramural Research Program of the NHLBI and NHGRI, NIH, and the National Center for Research Resources (NCRR) Grant M01-RR00039 for the Emory General Clinical Research Center (GCRC). Funding Information: Dr. Quyyumi has received research funding from Pfizer, which manufactures atorvastatin, a product related to the research described in this paper and has received honoraria as a consultant. The terms of this arrangement have been reviewed and approved by Emory University in accordance with its conflict of interest policies.

PY - 2010/10

Y1 - 2010/10

N2 - Objectives: The expression of FOS, a gene critical for monocyte and macrophage function, can be inhibited by statins through the disruption of a cholesterol-independent signaling pathway. In this pilot study, we hypothesized that blood FOS mRNA levels will be sensitive to statin treatment independent of LDL cholesterol levels. Methods: Three cohorts at increased risk of or with cardiovascular disease (CVD) were studied. Blood FOS mRNA levels were measured before and after statin treatment or in patients under stable treatment. Results: Statin treatment for three months significantly reduced blood FOS mRNA and LDL cholesterol levels. However, in subjects with similar LDL levels achieved by different doses of long term statin treatment, there was an inverse relationship between statin dose and FOS expression. Conclusions: FOS mRNA levels appear to be a sensitive marker of statin treatment that is dissociated from cholesterol levels.

AB - Objectives: The expression of FOS, a gene critical for monocyte and macrophage function, can be inhibited by statins through the disruption of a cholesterol-independent signaling pathway. In this pilot study, we hypothesized that blood FOS mRNA levels will be sensitive to statin treatment independent of LDL cholesterol levels. Methods: Three cohorts at increased risk of or with cardiovascular disease (CVD) were studied. Blood FOS mRNA levels were measured before and after statin treatment or in patients under stable treatment. Results: Statin treatment for three months significantly reduced blood FOS mRNA and LDL cholesterol levels. However, in subjects with similar LDL levels achieved by different doses of long term statin treatment, there was an inverse relationship between statin dose and FOS expression. Conclusions: FOS mRNA levels appear to be a sensitive marker of statin treatment that is dissociated from cholesterol levels.

KW - Atherosclerosis

KW - Biomarker

KW - Blood

KW - FOS

KW - Gene expression

KW - Inflammation

KW - Macrophage

KW - Monocyte

KW - Pleiotropic

KW - Statin

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U2 - 10.1016/j.atherosclerosis.2010.06.023

DO - 10.1016/j.atherosclerosis.2010.06.023

M3 - Article

C2 - 20619839

AN - SCOPUS:77957709876

SN - 0021-9150

VL - 212

SP - 567

EP - 570

JO - Atherosclerosis

JF - Atherosclerosis

IS - 2

ER -

FOS expression in blood as a LDL-independent marker of statin treatment

Abstract

Keywords

ASJC Scopus subject areas

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