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Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis

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Sorensen, Grith L ; Bladbjerg, Else Marie ; Steffensen, Rudi ; Tan, Qihua ; Madsen, Jens ; Drivsholm, Thomas ; Holmskov, Uffe. / Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis. In: Atherosclerosis. 2016 ; Vol. 246. pp. 7-12.

Bibtex

@article{31da0f100adf481e939d3b25fdcc681f,
title = "Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis",
abstract = "OBJECTIVE: Surfactant protein D (SP-D) is a defense collectin with inflammation-modulating properties. SP-D deficiency inhibits atherosclerosis in vivo, and the circulatory SP-D levels have been previously associated with cardiovascular disease mortality. We hypothesized that plasma SP-D (pSP-D) and SP-D gene (SFTPD) single nucleotide polymorphisms (SNPs) are risk factors for atherosclerosis.METHODS: We evaluated individuals who were all 60 years old and participated in The Glostrup Population Study. Subclinical atherosclerosis was diagnosed based on the ultrasonographic measurement of intima-media thickness (IMT) and protruding plaques in the right carotid artery. Associations between cardiovascular traits and the levels of pSP-D (n = 687) or two coding SFTPD SNPs rs3088308 and rs721917 (n = 396) were investigated using multiple linear regressions and logistic regressions.RESULTS: There was no significant association between pSP-D and the presence of plaques or IMT. The SFTPD SNP rs3088308 was nominally associated with the presence of plaques, and rs721917 was nominally associated with IMT. The directions of effects of associations were markedly dependent on current smoking status.CONCLUSIONS: The results do not support that pSP-D levels influence the development of subclinical atherosclerosis. However, the SFTPD SNP data support previous observations from animal studies that SP-D plays a role in the etiology of atherosclerotic disease development. The nominal significant effects are likely to be mediated by structural variant SP-D modulation of effects of tobacco smoking and are independent of pSP-D levels. The data warrant confirmation in larger cohorts.",
keywords = "Asymptomatic Diseases, Carotid Arteries, Carotid Artery Diseases, Carotid Intima-Media Thickness, Chi-Square Distribution, Denmark, Female, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Linear Models, Logistic Models, Male, Middle Aged, Multivariate Analysis, Phenotype, Plaque, Atherosclerotic, Polymorphism, Single Nucleotide, Pulmonary Surfactant-Associated Protein D, Risk Assessment, Risk Factors, Smoking, Journal Article, Research Support, Non-U.S. Gov't",
author = "Sorensen, {Grith L} and Bladbjerg, {Else Marie} and Rudi Steffensen and Qihua Tan and Jens Madsen and Thomas Drivsholm and Uffe Holmskov",
note = "Copyright {\circledC} 2015 Elsevier Ireland Ltd. All rights reserved.",
year = "2016",
month = "3",
doi = "10.1016/j.atherosclerosis.2015.12.037",
language = "English",
volume = "246",
pages = "7--12",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

T1 - Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis

AU - Sorensen, Grith L

AU - Bladbjerg, Else Marie

AU - Steffensen, Rudi

AU - Tan, Qihua

AU - Madsen, Jens

AU - Drivsholm, Thomas

AU - Holmskov, Uffe

N1 - Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

PY - 2016/3

Y1 - 2016/3

N2 - OBJECTIVE: Surfactant protein D (SP-D) is a defense collectin with inflammation-modulating properties. SP-D deficiency inhibits atherosclerosis in vivo, and the circulatory SP-D levels have been previously associated with cardiovascular disease mortality. We hypothesized that plasma SP-D (pSP-D) and SP-D gene (SFTPD) single nucleotide polymorphisms (SNPs) are risk factors for atherosclerosis.METHODS: We evaluated individuals who were all 60 years old and participated in The Glostrup Population Study. Subclinical atherosclerosis was diagnosed based on the ultrasonographic measurement of intima-media thickness (IMT) and protruding plaques in the right carotid artery. Associations between cardiovascular traits and the levels of pSP-D (n = 687) or two coding SFTPD SNPs rs3088308 and rs721917 (n = 396) were investigated using multiple linear regressions and logistic regressions.RESULTS: There was no significant association between pSP-D and the presence of plaques or IMT. The SFTPD SNP rs3088308 was nominally associated with the presence of plaques, and rs721917 was nominally associated with IMT. The directions of effects of associations were markedly dependent on current smoking status.CONCLUSIONS: The results do not support that pSP-D levels influence the development of subclinical atherosclerosis. However, the SFTPD SNP data support previous observations from animal studies that SP-D plays a role in the etiology of atherosclerotic disease development. The nominal significant effects are likely to be mediated by structural variant SP-D modulation of effects of tobacco smoking and are independent of pSP-D levels. The data warrant confirmation in larger cohorts.

AB - OBJECTIVE: Surfactant protein D (SP-D) is a defense collectin with inflammation-modulating properties. SP-D deficiency inhibits atherosclerosis in vivo, and the circulatory SP-D levels have been previously associated with cardiovascular disease mortality. We hypothesized that plasma SP-D (pSP-D) and SP-D gene (SFTPD) single nucleotide polymorphisms (SNPs) are risk factors for atherosclerosis.METHODS: We evaluated individuals who were all 60 years old and participated in The Glostrup Population Study. Subclinical atherosclerosis was diagnosed based on the ultrasonographic measurement of intima-media thickness (IMT) and protruding plaques in the right carotid artery. Associations between cardiovascular traits and the levels of pSP-D (n = 687) or two coding SFTPD SNPs rs3088308 and rs721917 (n = 396) were investigated using multiple linear regressions and logistic regressions.RESULTS: There was no significant association between pSP-D and the presence of plaques or IMT. The SFTPD SNP rs3088308 was nominally associated with the presence of plaques, and rs721917 was nominally associated with IMT. The directions of effects of associations were markedly dependent on current smoking status.CONCLUSIONS: The results do not support that pSP-D levels influence the development of subclinical atherosclerosis. However, the SFTPD SNP data support previous observations from animal studies that SP-D plays a role in the etiology of atherosclerotic disease development. The nominal significant effects are likely to be mediated by structural variant SP-D modulation of effects of tobacco smoking and are independent of pSP-D levels. The data warrant confirmation in larger cohorts.

KW - Asymptomatic Diseases

KW - Carotid Arteries

KW - Carotid Artery Diseases

KW - Carotid Intima-Media Thickness

KW - Chi-Square Distribution

KW - Denmark

KW - Female

KW - Genetic Association Studies

KW - Genetic Predisposition to Disease

KW - Humans

KW - Linear Models

KW - Logistic Models

KW - Male

KW - Middle Aged

KW - Multivariate Analysis

KW - Phenotype

KW - Plaque, Atherosclerotic

KW - Polymorphism, Single Nucleotide

KW - Pulmonary Surfactant-Associated Protein D

KW - Risk Assessment

KW - Risk Factors

KW - Smoking

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.atherosclerosis.2015.12.037

DO - 10.1016/j.atherosclerosis.2015.12.037

M3 - Journal article

VL - 246

SP - 7

EP - 12

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

ER -

ID: 49935312