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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

Atherosclerosis is attenuated by limiting superoxide generation in both macrophages and vessel wall cells

Aleksandr E Vendrov1, Zeenat S Hakim, Nageswara R Madamanchi

  • 1Department of Medicine, University of North Carolina at Chapel Hill, 3033 Old Clinic Building, Chapel Hill, NC 27599-7005, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|September 8, 2007
PubMed

Insights

Both monocyte/macrophages and vascular wall cells contribute to atherosclerosis by generating superoxide. Inhibiting NAD(P)H oxidase in either cell type reduced atherosclerotic lesions and related signaling in mice.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Immunology

Background:

  • NAD(P)H oxidase plays a significant role in reducing atherosclerosis in apoE(-/-) mice.
  • The specific contribution of NAD(P)H oxidase in different cell types to atherogenesis requires further elucidation.

Purpose of the Study:

  • To determine the distinct roles of monocyte/macrophage and vascular wall cell NAD(P)H oxidase in the development of atherosclerosis.
  • To investigate the impact of cell-specific NAD(P)H oxidase inhibition on atherosclerotic lesion formation and associated molecular pathways.

Main Methods:

  • Utilized allogenic, sex-mismatched bone marrow transplantation in apoE(-/-) mice to achieve cell-specific NAD(P)H oxidase inhibition.
  • Compared atherosclerotic burden, superoxide production, oxidized LDL levels, and cellular adhesion molecule expression in control, monocyte/macrophage-deficient (BMO), and vessel wall-deficient (VWO) mice.
  • Assessed neointimal hyperplasia and mitogenic protein activation following arterial injury in NAD(P)H oxidase-deficient mice.

Main Results:

  • Both BMO and VWO mice exhibited significantly reduced superoxide production and aortic atherosclerotic lesions compared to control mice.
  • BMO mice showed lower plasma oxidized LDL, while VWO mice displayed decreased cellular adhesion molecule expression.
  • NAD(P)H oxidase deficiency attenuated neointimal hyperplasia and mitogenic protein activation post-arterial injury.

Conclusions:

  • Monocyte/macrophages and vascular wall cells critically contribute to atherogenesis through distinct mechanisms.
  • Attenuated superoxide generation in either cell type significantly reduces atherosclerosis.
  • Superoxide generation influences atherosclerosis partly by activating smooth muscle cell mitogenic signaling.
Abstract

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