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Atherosclerosis/Lipoproteins

Loss of Id3 Increases VCAM-1 Expression, Macrophage Accumulation, and Atherogenesis in Ldlr−/− Mice

Michael J. Lipinski, Kirsti A. Campbell, Son Q. Duong, Thomas J. Welch, James C. Garmey, Amanda C. Doran, Marcus D. Skaflen, Stephanie N. Oldham, Kimberly A. Kelly, Coleen A. McNamara
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https://doi.org/10.1161/ATVBAHA.112.300352
Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;ATVBAHA.112.300352
Originally published October 4, 2012
Michael J. Lipinski
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Kirsti A. Campbell
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Son Q. Duong
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Thomas J. Welch
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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James C. Garmey
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Amanda C. Doran
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Marcus D. Skaflen
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Stephanie N. Oldham
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Kimberly A. Kelly
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Coleen A. McNamara
From the Cardiovascular Research Center (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D. M.D.S., S.N.O., K.A.K., C.A.M.), Department of Medicine, Cardiovascular Division (M.J.L., K.A.C., S.Q.D., T.J.W., J.C.G., A.C.D., M.D.S., S.N.O., C.A.M.), Department of Molecular Physiology and Biological Physics (M.J.L., A.C.D., C.A.M.), and the Department of Biomedical Engineering (K.A.K.), University of Virginia, Charlottesville, VA.
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Abstract

Objective—Inhibitor of differention-3 (Id3) promotes B cells homing to the aorta and atheroprotection in Apoe−/− mice. We sought to determine the impact of loss of Id3 in the Ldlr−/− mouse model of diet-induced atherosclerosis and identify novel Id3 targets in the vessel wall.

Methods and Results—Ex vivo optical imaging confirmed that Id3−/− Ldlr−/− mice have significantly fewer aortic B cells than Id3+/+ Ldlr−/− mice. After 8 and 16 weeks of Western diet, Id3−/− Ldlr−/− mice developed significantly more atherosclerosis than Id3+/+ Ldlr−/− mice, with Id3+/− Ldlr−/− mice demonstrating an intermediate phenotype. There were no differences in serum lipid levels between genotypes. Immunostaining demonstrated that aortas from Id3−/− Ldlr−/− mice had greater intimal macrophage density and CCL 20 and vascular cell adhesion molecule 1 (VCAM-1) expression compared with Id3+/+ Ldlr−/− mice. Real-time polymerase chain reaction demonstrated increased VCAM-1 mRNA levels in the aortas of Id3−/− Ldlr−/− mice. Primary vascular smooth muscle cells from Id3−/− mice expressed greater amounts of VCAM-1 protein compared with control. Gain and loss of function studies in primary vascular smooth muscle cells identified a role for Id3 in repressing VCAM-1 promoter activation. Chromatin immunoprecipitation demonstrated interaction of E12 with the VCAM-1 promoter, which is inhibited by Id3.

Conclusion—Id3 is an atheroprotective transcription regulator with targets in both B cells and vessel wall cells leading to reduced macrophages accumulation and reduced atherosclerosis formation.

  • Received March 30, 2012.
  • Accepted September 7, 2012.
  • © 2012 American Heart Association, Inc.
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    Loss of Id3 Increases VCAM-1 Expression, Macrophage Accumulation, and Atherogenesis in Ldlr−/− Mice
    Michael J. Lipinski, Kirsti A. Campbell, Son Q. Duong, Thomas J. Welch, James C. Garmey, Amanda C. Doran, Marcus D. Skaflen, Stephanie N. Oldham, Kimberly A. Kelly and Coleen A. McNamara
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;ATVBAHA.112.300352, originally published October 4, 2012
    https://doi.org/10.1161/ATVBAHA.112.300352

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    Loss of Id3 Increases VCAM-1 Expression, Macrophage Accumulation, and Atherogenesis in Ldlr−/− Mice
    Michael J. Lipinski, Kirsti A. Campbell, Son Q. Duong, Thomas J. Welch, James C. Garmey, Amanda C. Doran, Marcus D. Skaflen, Stephanie N. Oldham, Kimberly A. Kelly and Coleen A. McNamara
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;ATVBAHA.112.300352, originally published October 4, 2012
    https://doi.org/10.1161/ATVBAHA.112.300352
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