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Cardiovascular Research 2006 72(2):349-357; doi:10.1016/j.cardiores.2006.08.008
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Copyright © 2006, European Society of Cardiology

Carotid arterial stiffness, elastic fibre network and vasoreactivity in semicarbazide-sensitive amine-oxidase null mouse

Nathalie Merciera,b, Mary Osborne-Pellegrinc, Khadija El Hadrid, Augustine Kakoua, Carlos Labata, Laurent Loufranie, Daniel Henrione, Pascal Challandef, Sirpa Jalkanenb, Bruno Fèveg and Patrick Lacolleya,*

aINSERM U684, Vandoeuvre-les-Nancy, France
bMediCity Research Laboratory, University of Turku and National Public Health Institute, Turku, Finland
cINSERM U698, Paris, France
dUMR 7079 CNRS, Paris, France
eUMR-CNRS 6188, Angers, France
fUniversité Pierre et Marie Curie-Paris 6, FRE 2867 Saint-Cyr-l'Ecole, France
gINSERM U693, Le Kremlin-Bicêtre, France

* Corresponding author. INSERM U684, Faculté de Médecine, 9 Avenue de la Forêt de Haye, BP 184, 54505 Vandoeuvre-les-Nancy, Cedex, France. Tel.: +33 3 83 68 36 23; fax: +33 3 83 68 36 39. Email address: patrick.lacolley{at}nancy.inserm.fr

Objective: We examined the arterial phenotype of semicarbazide-sensitive amine-oxidase null mouse (SSAO –/–) using various techniques including high resolution echotracking.

Methods and results: SSAO –/– mice showed no change in arterial pressure under anesthesia. The in vivo arterial diameter, only measured in the carotid artery (CA), was higher in SSAO –/– than in SSAO +/+ animals. Elastic modulus–wall stress curves and CA rupture pressure were similar between SSAO –/– and +/+ mice, indicating no change in arterial wall stiffness or mechanical strength. There was no significant difference in insoluble elastin, total collagen content and elastic lamellar morphology between the two genotypes. No alteration in vascular reactivity was observed in aortic rings and mesenteric arteries from SSAO –/– mice. Aortic lysyl oxidase (LO) activity remained unaltered, indicating that SSAO invalidation is not accompanied by a compensatory increase in LO activity.

Conclusion: This is the first functional study of arteries lacking SSAO. Our results indicate that SSAO –/– mice present an increased arterial diameter associated with normal arterial mechanical properties, suggesting that SSAO deficiency might contribute to arterial wall remodeling. However, these results argue against the hypothesis that SSAO intervenes in elastic fibre organization, elastin cross-linking processes and vasoreactivity.

KEYWORDS Amine oxidase; Arterial stiffness; Elastin; Gene invalidation; SSAO; Vascular smooth muscle cells

Time for primary review 29 days


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