Association of a Vcam1 mutation with atherosclerosis susceptibility in diet-induced models of atherosclerosis

Toru Miyoshi; Zuobiao Yuan; Weibin Shi

doi:10.1016/j.atherosclerosis.2007.05.004

Association of a Vcam1 mutation with atherosclerosis susceptibility in diet-induced models of atherosclerosis

Toru Miyoshi, Zuobiao Yuan, Weibin Shi

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7 Scopus citations

Abstract

We previously identified a G > A single nucleotide polymorphism (SNP) between C57BL/6J (B6) and C3H/HeJ (C3H) mouse strains at position 2077 in the coding region of Vcam1 that leads to substitution of an amino acid from aspartic acid (D) to asparagine (N) in the protein product. In the present study, we investigated the association of this SNP with atherosclerosis susceptibility using a panel of inbred mouse strains, a set of recombinant inbred (RI) strains derived from B6 and C3H mice, and a cohort of F2 mice derived from B6 and C3H apolipoprotein E-deficient (apoE^-/-) mice. Inbred strain analysis revealed that mouse strains with the B6 Vcam1 genotype developed significantly larger atherosclerotic lesions than strains with the C3H genotype (4622 ± 2816 μm²/section versus 362 ± 697 μm²/section; P = 0.029). BXH RI strains with the B6 Vcam1 genotype also developed larger atherosclerotic lesions than those with the C3H genotype (8305 ± 9031 μm²/section versus 2139 ± 2931 μm²/section) although the difference was not statistically significant (P = 0.13). In contrast, no association was detected between Vcam1 and atherosclerotic lesion size in F2 mice. The present data indicate that the G > A mutation of Vcam1 is associated with atherosclerotic lesion formation in the dietary but not apoE^-/- models of atherosclerosis and this association suggests a role for the Vcam1 gene in influencing atherosclerosis susceptibility.

Original language	English (US)
Pages (from-to)	234-239
Number of pages	6
Journal	Atherosclerosis
Volume	196
Issue number	1
DOIs	https://doi.org/10.1016/j.atherosclerosis.2007.05.004
State	Published - Jan 2008
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by National Institutes of Health grants HL71844 and HL75433. The authors thank Jessica Rowlan for critically reviewing the manuscript.

Keywords

Atherosclerosis
Mouse
Single nucleotide polymorphism
Vcam1

UN SDGs

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

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10.1016/j.atherosclerosis.2007.05.004

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title = "Association of a Vcam1 mutation with atherosclerosis susceptibility in diet-induced models of atherosclerosis",

abstract = "We previously identified a G > A single nucleotide polymorphism (SNP) between C57BL/6J (B6) and C3H/HeJ (C3H) mouse strains at position 2077 in the coding region of Vcam1 that leads to substitution of an amino acid from aspartic acid (D) to asparagine (N) in the protein product. In the present study, we investigated the association of this SNP with atherosclerosis susceptibility using a panel of inbred mouse strains, a set of recombinant inbred (RI) strains derived from B6 and C3H mice, and a cohort of F2 mice derived from B6 and C3H apolipoprotein E-deficient (apoE-/-) mice. Inbred strain analysis revealed that mouse strains with the B6 Vcam1 genotype developed significantly larger atherosclerotic lesions than strains with the C3H genotype (4622 ± 2816 μm2/section versus 362 ± 697 μm2/section; P = 0.029). BXH RI strains with the B6 Vcam1 genotype also developed larger atherosclerotic lesions than those with the C3H genotype (8305 ± 9031 μm2/section versus 2139 ± 2931 μm2/section) although the difference was not statistically significant (P = 0.13). In contrast, no association was detected between Vcam1 and atherosclerotic lesion size in F2 mice. The present data indicate that the G > A mutation of Vcam1 is associated with atherosclerotic lesion formation in the dietary but not apoE-/- models of atherosclerosis and this association suggests a role for the Vcam1 gene in influencing atherosclerosis susceptibility.",

keywords = "Atherosclerosis, Mouse, Single nucleotide polymorphism, Vcam1",

author = "Toru Miyoshi and Zuobiao Yuan and Weibin Shi",

note = "Funding Information: This work was supported by National Institutes of Health grants HL71844 and HL75433. The authors thank Jessica Rowlan for critically reviewing the manuscript.",

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doi = "10.1016/j.atherosclerosis.2007.05.004",

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AU - Miyoshi, Toru

AU - Yuan, Zuobiao

AU - Shi, Weibin

N1 - Funding Information: This work was supported by National Institutes of Health grants HL71844 and HL75433. The authors thank Jessica Rowlan for critically reviewing the manuscript.

PY - 2008/1

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N2 - We previously identified a G > A single nucleotide polymorphism (SNP) between C57BL/6J (B6) and C3H/HeJ (C3H) mouse strains at position 2077 in the coding region of Vcam1 that leads to substitution of an amino acid from aspartic acid (D) to asparagine (N) in the protein product. In the present study, we investigated the association of this SNP with atherosclerosis susceptibility using a panel of inbred mouse strains, a set of recombinant inbred (RI) strains derived from B6 and C3H mice, and a cohort of F2 mice derived from B6 and C3H apolipoprotein E-deficient (apoE-/-) mice. Inbred strain analysis revealed that mouse strains with the B6 Vcam1 genotype developed significantly larger atherosclerotic lesions than strains with the C3H genotype (4622 ± 2816 μm2/section versus 362 ± 697 μm2/section; P = 0.029). BXH RI strains with the B6 Vcam1 genotype also developed larger atherosclerotic lesions than those with the C3H genotype (8305 ± 9031 μm2/section versus 2139 ± 2931 μm2/section) although the difference was not statistically significant (P = 0.13). In contrast, no association was detected between Vcam1 and atherosclerotic lesion size in F2 mice. The present data indicate that the G > A mutation of Vcam1 is associated with atherosclerotic lesion formation in the dietary but not apoE-/- models of atherosclerosis and this association suggests a role for the Vcam1 gene in influencing atherosclerosis susceptibility.

AB - We previously identified a G > A single nucleotide polymorphism (SNP) between C57BL/6J (B6) and C3H/HeJ (C3H) mouse strains at position 2077 in the coding region of Vcam1 that leads to substitution of an amino acid from aspartic acid (D) to asparagine (N) in the protein product. In the present study, we investigated the association of this SNP with atherosclerosis susceptibility using a panel of inbred mouse strains, a set of recombinant inbred (RI) strains derived from B6 and C3H mice, and a cohort of F2 mice derived from B6 and C3H apolipoprotein E-deficient (apoE-/-) mice. Inbred strain analysis revealed that mouse strains with the B6 Vcam1 genotype developed significantly larger atherosclerotic lesions than strains with the C3H genotype (4622 ± 2816 μm2/section versus 362 ± 697 μm2/section; P = 0.029). BXH RI strains with the B6 Vcam1 genotype also developed larger atherosclerotic lesions than those with the C3H genotype (8305 ± 9031 μm2/section versus 2139 ± 2931 μm2/section) although the difference was not statistically significant (P = 0.13). In contrast, no association was detected between Vcam1 and atherosclerotic lesion size in F2 mice. The present data indicate that the G > A mutation of Vcam1 is associated with atherosclerotic lesion formation in the dietary but not apoE-/- models of atherosclerosis and this association suggests a role for the Vcam1 gene in influencing atherosclerosis susceptibility.

KW - Atherosclerosis

KW - Mouse

KW - Single nucleotide polymorphism

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Association of a Vcam1 mutation with atherosclerosis susceptibility in diet-induced models of atherosclerosis

Abstract

Bibliographical note

Keywords

UN SDGs

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