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Author Notes:

Ada Lee and Pete Correll Professor Coulter Department of Biomedical Engineering Department of Medicine, Division of Cardiology, Georgia Institute of Technology and Emory University Woodruff Memorial Bldg, Rm 2005 Atlanta, GA 30322 Phone: 404-712-9654 Fax: 404-727-9873 hjo@bme.gatech.edu.

N.A.G. and A.R. contributed equally to this work.

Authors had no disclosures.

Subjects:

Research Funding:

Work supported by funding from NIH grants HL095070, HL70531, HHSN268201000043C; and a World Class University Project in Korea (R31-2008-000-10010-0) to HJ.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Hematology
  • Peripheral Vascular Disease
  • Cardiovascular System & Cardiology
  • atherosclerosis
  • leukocytes
  • disturbed flow
  • flow cytometry
  • inflammation
  • ACUTE CORONARY SYNDROMES
  • SMOOTH-MUSCLE-CELLS
  • T-CELL
  • DISTURBED FLOW
  • ATHEROSCLEROTIC PLAQUES
  • INDUCED APOPTOSIS
  • INTERFERON-GAMMA
  • APOE(-/-) MICE
  • DEFICIENT MICE
  • NITRIC-OXIDE

Dynamic Immune Cell Accumulation During Flow-Induced Atherogenesis in Mouse Carotid Artery An Expanded Flow Cytometry Method

Tools:

Journal Title:

Arteriosclerosis, Thrombosis, and Vascular Biology

Volume:

Volume 32, Number 3

Publisher:

, Pages 623-U217

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Objective-Inflammation plays a central role in atherosclerosis. However, the detailed changes in the composition and quantity of leukocytes in the arterial wall during atherogenesis are not fully understood in part because of the lack of suitable methods and animal models. Methods and Results-We developed a 10-fluorochrome, 13-parameter flow cytometry method to quantitate 7 major leukocyte subsets in a single digested arterial wall sample. Apolipoprotein E-deficient mice underwent left carotid artery (LCA) partial ligation and were fed a high-fat diet for 4 to 28 days. Monocyte/macrophages, dendritic cells, granulocytes, natural killer cells, and CD4 T cells significantly infiltrated the LCA as early as 4 days. Monocyte/macrophages and dendritic cells decreased between 7 and 14 days, whereas T-cell numbers remained steady. Leukocyte numbers peaked at 7 days, preceding atheroma formation at 14 days. B cells entered LCA by 14 days. Control right carotid and sham-ligated LCAs showed no significant infiltrates. Polymerase chain reaction and ELISA arrays showed that expression of proinflammatory cytokines and chemokines peaked at 7 and 14 days postligation, respectively. Conclusion-This is the first quantitative description of leukocyte number and composition over the life span of murine atherosclerosis. These results show that disturbed flow induces rapid and dynamic leukocyte accumulation in the arterial wall during the initiation and progression of atherosclerosis.

Copyright information:

© 2012 American Heart Association, Inc.

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