Research article summary (published 12 Aug 2009):

Partial carotid ligation is a model of acutely induced disturbed flow, leading to rapid endothelial dysfunction and atherosclerosis.

Full Abstract

Atherosclerosis is closely associated with disturbed flow characterized by low and oscillatory shear stress, but studies directly linking disturbed flow to atherogenesis is lacking. The major reason for this has been a lack of an animal model in which disturbed flow can be acutely induced and cause atherosclerosis. Here, we characterize partial carotid ligation as a model of disturbed flow with characteristics of low and oscillatory wall shear stress. We also describe a method of isolating intimal RNA in sufficient quantity from mouse carotid arteries. Using this model and method, we found that partial ligation causes upregulation of proatherogenic genes, downregulation of antiatherogenic genes, endothelial dysfunction, and rapid atherosclerosis in 2 wk in a p47(phox)-dependent manner and advanced lesions by 4 wk. We found that partial ligation results in endothelial dysfunction, rapid atherosclerosis, and advanced lesion development in a physiologically relevant model of disturbed flow. It also allows for easy and rapid intimal RNA isolation. This novel model and method could be used for genome-wide studies to determine molecular mechanisms underlying flow-dependent regulation of vascular biology and diseases.

Author information

Author/s: Nam, Douglas (D); Ni, Chih-Wen (CW); Rezvan, Amir (A); Suo, Jin (J); Budzyn, Klaudia (K); Llanos, Alexander (A); Harrison, David (D); Giddens, Don (D); Jo, Hanjoong (H);

Affiliation: Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA.

Grants: HL-75209 (Agency:NHLBI NIH HHS) ; HL-87012 (Agency:NHLBI NIH HHS) ; UO1HL-80711 (Agency:NHLBI NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

Journal: American journal of physiology. Heart and circulatory physiology (Am J Physiol Heart Circ Physiol), published in United States. (Language: eng)

Reference: 2009-Oct; vol 297 (issue 4) : pp H1535-43

Dates: Created 2009/09/25; Completed 2009/10/08;

PMID: 19684185, status: MEDLINE (last retrieval date: 10/8/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Apolipoproteins E - deficiency; genetics Carotid Arteries - drug effects; metabolism; pathology; physiopathology; surgery Carotid Artery Diseases - etiology; genetics; pathology; physiopathology Computer Simulation Dietary Fats - administration & dosage Disease Models, Animal Disease Progression Dose-Response Relationship, Drug Endothelium, Vascular - drug effects; pathology; physiopathology Female Gene Expression Regulation Ligation Male

Male Mice Mice, Inbred C57BL Mice, Knockout Models, Cardiovascular NADPH Oxidase - deficiency; genetics RNA - isolation & purification Regional Blood Flow Stress, Mechanical Superoxides - metabolism Time Factors Tunica Intima - metabolism; pathology; physiopathology Vasodilation Vasodilator Agents - pharmacology

Associated Chemicals: Apolipoproteins E (0) ; Dietary Fats (0) ; Vasodilator Agents (0) ; Superoxides (11062-77-4) ; RNA (63231-63-0) ; NADPH Oxidase (EC 1.6.3.1) ; neutrophil cytosolic factor 1 (EC 1.6.3.1)

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