Abstract |
Endothelial dysfunction, defined as a deficit in the bioavailability of nitric oxide (NO), occurs as sequelae of many vascular diseases; however, the utility of supplementing NO to obviate the extent of disease is understudied. Here, we examined if prolonged treatment with an NO-releasing form of aspirin ( NO-ASA) can influence neointimal remodeling of femoral arteries of hypercholesterolemic ApoE (-/-) mice. Treatment of ApoE (-/-) mice with NO-ASA, but not aspirin (ASA), improved neointimal remodeling post-injury. NO-ASA treatment increased lumen diameters and reduced intimal-to-medial ratios of injured femoral arteries compared with ASA- or vehicle-treated mice. The reduction in lumen diameter in NO-ASA-treated mice was associated with a marked reduction in CD45-positive inflammatory cells and an increased number of TUNEL-positive cells. Thus, NO-ASA, by virtue of releasing NO, can reduce vascular inflammation and promote apoptosis during vascular remodeling associated with neointimal thickening.
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Authors | Jun Yu, Radu Daniel Rudic, William C Sessa |
Journal | Laboratory investigation; a journal of technical methods and pathology
(Lab Invest)
Vol. 82
Issue 7
Pg. 825-32
(Jul 2002)
ISSN: 0023-6837 [Print] United States |
PMID | 12118084
(Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Apolipoproteins E
- Platelet Aggregation Inhibitors
- nitroxy-butyl-acetylsalicylic acid
- Cholesterol
- Aspirin
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Topics |
- Animals
- Apolipoproteins E
(deficiency)
- Apoptosis
(drug effects)
- Aspirin
(analogs & derivatives, pharmacology, therapeutic use)
- Cholesterol
(blood)
- Disease Models, Animal
- Femoral Artery
(drug effects, pathology)
- Humans
- Inflammation
(prevention & control)
- Male
- Mice
- Mice, Knockout
- Muscle, Smooth, Vascular
(drug effects, pathology)
- Platelet Aggregation Inhibitors
(therapeutic use)
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