Quantitative genetic analysis of cellular adhesion molecules: The Fels Longitudinal Study

Miryoung Lee; Stefan A. Czerwinski; Audrey C. Choh; Ellen W. Demerath; Shumei S. Sun; Wm C. Chumlea; Bradford Towne; Roger M. Siervogel

doi:10.1016/j.atherosclerosis.2005.05.027

Quantitative genetic analysis of cellular adhesion molecules: The Fels Longitudinal Study

Miryoung Lee, Stefan A. Czerwinski, Audrey C. Choh, Ellen W. Demerath, Shumei S. Sun, Wm C. Chumlea, Bradford Towne, Roger M. Siervogel

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

12 Scopus citations

Abstract

Circulating concentrations of inflammatory markers predict cardiovascular disease (CVD) risk and are closely associated with obesity. However, little is known concerning genetic influences on serum levels of inflammatory markers. In this study, we estimated the heritability (h²) of soluble cellular adhesion molecule (sCAM) concentrations and examined the correlational architecture between different sCAMs. The study population included 234 men and 270 women aged 18-76 years, belonging to 121 families participating in the Fels Longitudinal Study. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sESEL-1) and P-selectin (sPSEL-1) were assayed using commercially available kits. A variance components-based maximum likelihood method was used to estimate the h ² of the different serum inflammatory markers while simultaneously adjusting for the effects of known CVD risk factors, such as age and smoking. Additionally, we used bivariate extensions of these methods to estimate genetic and random environmental correlations among sCAMs. Levels of sCAMs were significantly heritable: h² = 0.24 ± 0.10 for sICAM-1, h ² = 0.22 ± 0.10 for sVCAM-1, h² = 0.50 ± 0.11 for sESEL-1, and h² = 0.46 ± 0.10 for sPSEL-1. In addition, a significant genetic correlation (ρ_G = 0.63) was found between sICAM-1 and sVCAM-1 indicating some degree of shared genetic control. In the Fels Longitudinal Study, the levels of four sCAMs are significantly influenced by genetic effects, and sICAM-1 shares a common genetic background with sVCAM-1.

Original language	English (US)
Pages (from-to)	150-158
Number of pages	9
Journal	Atherosclerosis
Volume	185
Issue number	1
DOIs	https://doi.org/10.1016/j.atherosclerosis.2005.05.027
State	Published - Mar 2006

Bibliographical note

Funding Information:
We are grateful for the participation of the families in the Fels Longitudinal Study and the assistance of our research staff. We also thank Dr. John Blangero and his staff for conducting the assays of sCAMs. This study was supported by National Institutes of Health grants (HD12252, HL69995, DK064391, DK64870), and an American Heart Association postdoctoral fellowship grant (0325311B). This study was presented in part at the American Heart Association 44th Annual Conference on Cardiovascular Disease Epidemiology and Prevention in 2004.

Keywords

Cell adhesion molecules
Family study
Genetic correlation
Heritability
Inflammatory markers

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.atherosclerosis.2005.05.027

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@article{c51fc577a803415da9f05e46b82492af,

title = "Quantitative genetic analysis of cellular adhesion molecules: The Fels Longitudinal Study",

abstract = "Circulating concentrations of inflammatory markers predict cardiovascular disease (CVD) risk and are closely associated with obesity. However, little is known concerning genetic influences on serum levels of inflammatory markers. In this study, we estimated the heritability (h2) of soluble cellular adhesion molecule (sCAM) concentrations and examined the correlational architecture between different sCAMs. The study population included 234 men and 270 women aged 18-76 years, belonging to 121 families participating in the Fels Longitudinal Study. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sESEL-1) and P-selectin (sPSEL-1) were assayed using commercially available kits. A variance components-based maximum likelihood method was used to estimate the h 2 of the different serum inflammatory markers while simultaneously adjusting for the effects of known CVD risk factors, such as age and smoking. Additionally, we used bivariate extensions of these methods to estimate genetic and random environmental correlations among sCAMs. Levels of sCAMs were significantly heritable: h2 = 0.24 ± 0.10 for sICAM-1, h 2 = 0.22 ± 0.10 for sVCAM-1, h2 = 0.50 ± 0.11 for sESEL-1, and h2 = 0.46 ± 0.10 for sPSEL-1. In addition, a significant genetic correlation (ρG = 0.63) was found between sICAM-1 and sVCAM-1 indicating some degree of shared genetic control. In the Fels Longitudinal Study, the levels of four sCAMs are significantly influenced by genetic effects, and sICAM-1 shares a common genetic background with sVCAM-1.",

keywords = "Cell adhesion molecules, Family study, Genetic correlation, Heritability, Inflammatory markers",

author = "Miryoung Lee and Czerwinski, {Stefan A.} and Choh, {Audrey C.} and Demerath, {Ellen W.} and Sun, {Shumei S.} and Chumlea, {Wm C.} and Bradford Towne and Siervogel, {Roger M.}",

note = "Funding Information: We are grateful for the participation of the families in the Fels Longitudinal Study and the assistance of our research staff. We also thank Dr. John Blangero and his staff for conducting the assays of sCAMs. This study was supported by National Institutes of Health grants (HD12252, HL69995, DK064391, DK64870), and an American Heart Association postdoctoral fellowship grant (0325311B). This study was presented in part at the American Heart Association 44th Annual Conference on Cardiovascular Disease Epidemiology and Prevention in 2004.",

year = "2006",

month = mar,

doi = "10.1016/j.atherosclerosis.2005.05.027",

language = "English (US)",

volume = "185",

pages = "150--158",

journal = "Atherosclerosis",

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AU - Lee, Miryoung

AU - Czerwinski, Stefan A.

AU - Choh, Audrey C.

AU - Demerath, Ellen W.

AU - Sun, Shumei S.

AU - Chumlea, Wm C.

AU - Towne, Bradford

AU - Siervogel, Roger M.

N1 - Funding Information: We are grateful for the participation of the families in the Fels Longitudinal Study and the assistance of our research staff. We also thank Dr. John Blangero and his staff for conducting the assays of sCAMs. This study was supported by National Institutes of Health grants (HD12252, HL69995, DK064391, DK64870), and an American Heart Association postdoctoral fellowship grant (0325311B). This study was presented in part at the American Heart Association 44th Annual Conference on Cardiovascular Disease Epidemiology and Prevention in 2004.

PY - 2006/3

Y1 - 2006/3

N2 - Circulating concentrations of inflammatory markers predict cardiovascular disease (CVD) risk and are closely associated with obesity. However, little is known concerning genetic influences on serum levels of inflammatory markers. In this study, we estimated the heritability (h2) of soluble cellular adhesion molecule (sCAM) concentrations and examined the correlational architecture between different sCAMs. The study population included 234 men and 270 women aged 18-76 years, belonging to 121 families participating in the Fels Longitudinal Study. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sESEL-1) and P-selectin (sPSEL-1) were assayed using commercially available kits. A variance components-based maximum likelihood method was used to estimate the h 2 of the different serum inflammatory markers while simultaneously adjusting for the effects of known CVD risk factors, such as age and smoking. Additionally, we used bivariate extensions of these methods to estimate genetic and random environmental correlations among sCAMs. Levels of sCAMs were significantly heritable: h2 = 0.24 ± 0.10 for sICAM-1, h 2 = 0.22 ± 0.10 for sVCAM-1, h2 = 0.50 ± 0.11 for sESEL-1, and h2 = 0.46 ± 0.10 for sPSEL-1. In addition, a significant genetic correlation (ρG = 0.63) was found between sICAM-1 and sVCAM-1 indicating some degree of shared genetic control. In the Fels Longitudinal Study, the levels of four sCAMs are significantly influenced by genetic effects, and sICAM-1 shares a common genetic background with sVCAM-1.

AB - Circulating concentrations of inflammatory markers predict cardiovascular disease (CVD) risk and are closely associated with obesity. However, little is known concerning genetic influences on serum levels of inflammatory markers. In this study, we estimated the heritability (h2) of soluble cellular adhesion molecule (sCAM) concentrations and examined the correlational architecture between different sCAMs. The study population included 234 men and 270 women aged 18-76 years, belonging to 121 families participating in the Fels Longitudinal Study. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sESEL-1) and P-selectin (sPSEL-1) were assayed using commercially available kits. A variance components-based maximum likelihood method was used to estimate the h 2 of the different serum inflammatory markers while simultaneously adjusting for the effects of known CVD risk factors, such as age and smoking. Additionally, we used bivariate extensions of these methods to estimate genetic and random environmental correlations among sCAMs. Levels of sCAMs were significantly heritable: h2 = 0.24 ± 0.10 for sICAM-1, h 2 = 0.22 ± 0.10 for sVCAM-1, h2 = 0.50 ± 0.11 for sESEL-1, and h2 = 0.46 ± 0.10 for sPSEL-1. In addition, a significant genetic correlation (ρG = 0.63) was found between sICAM-1 and sVCAM-1 indicating some degree of shared genetic control. In the Fels Longitudinal Study, the levels of four sCAMs are significantly influenced by genetic effects, and sICAM-1 shares a common genetic background with sVCAM-1.

KW - Cell adhesion molecules

KW - Family study

KW - Genetic correlation

KW - Heritability

KW - Inflammatory markers

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JO - Atherosclerosis

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ER -

Quantitative genetic analysis of cellular adhesion molecules: The Fels Longitudinal Study

Abstract

Bibliographical note

Keywords

UN SDGs

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